Trained immunity: A program of innate immune memory in health and disease
Classical immunological memory, carried out by T and B lymphocytes, ensures that we feel the ill effects of many pathogens only once. Netea et al.review how cells of the innate immune system, which lack the antigen specificity, clonality, and longevity of T cell and B cells, have some capacity to re...
Ausführliche Beschreibung
Autor*in: |
Mihai G Netea [verfasserIn] |
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Format: |
Artikel |
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Sprache: |
Englisch |
Erschienen: |
2016 |
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Rechteinformationen: |
Nutzungsrecht: Copyright © 2016, American Association for the Advancement of Science. |
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Schlagwörter: |
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Übergeordnetes Werk: |
Enthalten in: Science - Washington, DC : AAAS, American Assoc. for the Advancement of Science, 1883, 352(2016), 6284 |
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Übergeordnetes Werk: |
volume:352 ; year:2016 ; number:6284 |
Links: |
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DOI / URN: |
10.1126/science.aaf1098 |
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Katalog-ID: |
OLC1975103874 |
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520 | |a Classical immunological memory, carried out by T and B lymphocytes, ensures that we feel the ill effects of many pathogens only once. Netea et al.review how cells of the innate immune system, which lack the antigen specificity, clonality, and longevity of T cell and B cells, have some capacity to remember, too. Termed "trained immunity," the property allows macrophages, monocytes, and natural killer cells to show enhanced responsiveness when they reencounter pathogens. Epigenetic changes largely drive trained immunity, which is shorter lived and less specific than classical memory but probably still gives us a leg up during many infections. Science, this issue p. 10.1126/science.aaf1098 Host immune responses are classically divided into innate immune responses, which react rapidly and nonspecifically upon encountering a pathogen, and adaptive immune responses, which are slower to develop but are specific and build up immunological memory. The dogma that only adaptive immunity can build immunological memory has recently been challenged by studies showing that innate immune responses in plants and invertebrates (organisms lacking adaptive immune responses) can mount resistance to reinfection. Furthermore, in certain mammalian models of vaccination, protection from reinfection has been shown to occur independently of T and B lymphocytes. These observations led to the hypothesis that innate immunity can display adaptive characteristics after challenge with pathogens or their products. This de facto immunological memory has been termed "trained immunity" or "innate immune memory." In recent years, emerging evidence has shown that after infection or vaccination, prototypical innate immune cells (such as monocytes, macrophages, or natural killer cells) display long-term changes in their functional programs. These changes lead to increased responsiveness upon secondary stimulation by microbial pathogens, increased production of inflammatory mediators, and enhanced capacity to eliminate infection. Mechanistic studies have demonstrated that trained immunity is based on epigenetic reprogramming, which is broadly defined as sustained changes in transcription programs and cell physiology that do not involve permanent genetic changes, such as mutations and recombination. Histone modifications with chromatin reconfiguration have proven to be a central process for trained immunity, but other mechanisms--such as DNA methylation or modulation of microRNA and/or long noncoding RNA expression--are also expected to be involved. This leads to transcriptional programs that rewire the intracellular immune signaling of innate immune cells but also induce a shift of cellular metabolism from oxidative phosphorylation toward aerobic glycolysis, thus increasing the innate immune cells' capacity to respond to stimulation. Trained immunity programs have evolved as adaptive states that enhance fitness of the host (e.g., protective effects after infection or vaccination, or induction of mucosal tolerance toward colonizing microorganisms). Proof-of-principle experimental studies support the hypothesis that trained immunity is one of the main immunological processes that mediate the nonspecific protective effects against infections induced by vaccines, such as bacillus Calmette-Guérin or measles vaccination. However, when inappropriately activated, trained immunity programs can become maladaptive, as in postsepsis immune paralysis or autoinflammatory diseases. The discovery of trained immunity has revealed an important and previously unrecognized property of human immune responses. This advance opens the door for future research to explore trained immunity's effect on disease, for both diseases with impaired host defense, such as postsepsis immune paralysis or cancers, and autoinflammatory diseases, in which there is inappropriate activation of inflammation. These findings have considerable potential for aiding in the design of new therapeutic strategies, such as new generations of vaccines that combine classical immunological memory and trained immunity, the activation of trained immunity for the treatment of postsepsis immune paralysis or other immune deficiency states, and modulation of exaggerated inflammation in autoinflammatory diseases. Trained immunity evolved to lead to adaptive states that protect the host during microbial colonization or after infections. However, in certain situations, trained immunity may result in maladaptive states such as postsepsis immune paralysis or hyperinflammation. miRNA, microRNA. The general view that only adaptive immunity can build immunological memory has recently been challenged. In organisms lacking adaptive immunity, as well as in mammals, the innate immune system can mount resistance to reinfection, a phenomenon termed "trained immunity" or "innate immune memory." Trained immunity is orchestrated by epigenetic reprogramming, broadly defined as sustained changes in gene expression and cell physiology that do not involve permanent genetic changes such as mutations and recombination, which are essential for adaptive immunity. The discovery of trained immunity may open the door for novel vaccine approaches, new therapeutic strategies for the treatment of immune deficiency states, and modulation of exaggerated inflammation in autoinflammatory diseases. | ||
540 | |a Nutzungsrecht: Copyright © 2016, American Association for the Advancement of Science. | ||
650 | 4 | |a Histones - metabolism | |
650 | 4 | |a Immunologic Memory - immunology | |
650 | 4 | |a Immunity, Innate - immunology | |
650 | 4 | |a Immunologic Memory - genetics | |
650 | 4 | |a Invertebrates - immunology | |
650 | 4 | |a Immunity, Innate - genetics | |
650 | 4 | |a Plants - immunology | |
650 | 4 | |a Vaccines - immunology | |
650 | 4 | |a Inflammation - immunology | |
650 | 4 | |a Infection - immunology | |
700 | 0 | |a Leo A B Joosten |4 oth | |
700 | 0 | |a Eicke Latz |4 oth | |
700 | 0 | |a Kingston H G Mills |4 oth | |
700 | 0 | |a Gioacchino Natoli |4 oth | |
700 | 0 | |a Hendrik G Stunnenberg |4 oth | |
700 | 0 | |a Luke A J O'Neill |4 oth | |
700 | 0 | |a Ramnik J Xavier |4 oth | |
773 | 0 | 8 | |i Enthalten in |t Science |d Washington, DC : AAAS, American Assoc. for the Advancement of Science, 1883 |g 352(2016), 6284 |w (DE-627)12931482X |w (DE-600)128410-1 |w (DE-576)014533189 |x 0036-8075 |7 nnns |
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10.1126/science.aaf1098 doi PQ20160610 (DE-627)OLC1975103874 (DE-599)GBVOLC1975103874 (PRQ)c1684-b2a624b1b5577820d4fb88e31621b33c4554976323e2a1ea7bb6181af8ed0f7a0 (KEY)0063888920160000352628400000trainedimmunityaprogramofinnateimmunememoryinhealt DE-627 ger DE-627 rakwb eng 500 DNB LING fid Mihai G Netea verfasserin aut Trained immunity: A program of innate immune memory in health and disease 2016 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier Classical immunological memory, carried out by T and B lymphocytes, ensures that we feel the ill effects of many pathogens only once. Netea et al.review how cells of the innate immune system, which lack the antigen specificity, clonality, and longevity of T cell and B cells, have some capacity to remember, too. Termed "trained immunity," the property allows macrophages, monocytes, and natural killer cells to show enhanced responsiveness when they reencounter pathogens. Epigenetic changes largely drive trained immunity, which is shorter lived and less specific than classical memory but probably still gives us a leg up during many infections. Science, this issue p. 10.1126/science.aaf1098 Host immune responses are classically divided into innate immune responses, which react rapidly and nonspecifically upon encountering a pathogen, and adaptive immune responses, which are slower to develop but are specific and build up immunological memory. The dogma that only adaptive immunity can build immunological memory has recently been challenged by studies showing that innate immune responses in plants and invertebrates (organisms lacking adaptive immune responses) can mount resistance to reinfection. Furthermore, in certain mammalian models of vaccination, protection from reinfection has been shown to occur independently of T and B lymphocytes. These observations led to the hypothesis that innate immunity can display adaptive characteristics after challenge with pathogens or their products. This de facto immunological memory has been termed "trained immunity" or "innate immune memory." In recent years, emerging evidence has shown that after infection or vaccination, prototypical innate immune cells (such as monocytes, macrophages, or natural killer cells) display long-term changes in their functional programs. These changes lead to increased responsiveness upon secondary stimulation by microbial pathogens, increased production of inflammatory mediators, and enhanced capacity to eliminate infection. Mechanistic studies have demonstrated that trained immunity is based on epigenetic reprogramming, which is broadly defined as sustained changes in transcription programs and cell physiology that do not involve permanent genetic changes, such as mutations and recombination. Histone modifications with chromatin reconfiguration have proven to be a central process for trained immunity, but other mechanisms--such as DNA methylation or modulation of microRNA and/or long noncoding RNA expression--are also expected to be involved. This leads to transcriptional programs that rewire the intracellular immune signaling of innate immune cells but also induce a shift of cellular metabolism from oxidative phosphorylation toward aerobic glycolysis, thus increasing the innate immune cells' capacity to respond to stimulation. Trained immunity programs have evolved as adaptive states that enhance fitness of the host (e.g., protective effects after infection or vaccination, or induction of mucosal tolerance toward colonizing microorganisms). Proof-of-principle experimental studies support the hypothesis that trained immunity is one of the main immunological processes that mediate the nonspecific protective effects against infections induced by vaccines, such as bacillus Calmette-Guérin or measles vaccination. However, when inappropriately activated, trained immunity programs can become maladaptive, as in postsepsis immune paralysis or autoinflammatory diseases. The discovery of trained immunity has revealed an important and previously unrecognized property of human immune responses. This advance opens the door for future research to explore trained immunity's effect on disease, for both diseases with impaired host defense, such as postsepsis immune paralysis or cancers, and autoinflammatory diseases, in which there is inappropriate activation of inflammation. These findings have considerable potential for aiding in the design of new therapeutic strategies, such as new generations of vaccines that combine classical immunological memory and trained immunity, the activation of trained immunity for the treatment of postsepsis immune paralysis or other immune deficiency states, and modulation of exaggerated inflammation in autoinflammatory diseases. Trained immunity evolved to lead to adaptive states that protect the host during microbial colonization or after infections. However, in certain situations, trained immunity may result in maladaptive states such as postsepsis immune paralysis or hyperinflammation. miRNA, microRNA. The general view that only adaptive immunity can build immunological memory has recently been challenged. In organisms lacking adaptive immunity, as well as in mammals, the innate immune system can mount resistance to reinfection, a phenomenon termed "trained immunity" or "innate immune memory." Trained immunity is orchestrated by epigenetic reprogramming, broadly defined as sustained changes in gene expression and cell physiology that do not involve permanent genetic changes such as mutations and recombination, which are essential for adaptive immunity. The discovery of trained immunity may open the door for novel vaccine approaches, new therapeutic strategies for the treatment of immune deficiency states, and modulation of exaggerated inflammation in autoinflammatory diseases. Nutzungsrecht: Copyright © 2016, American Association for the Advancement of Science. Histones - metabolism Immunologic Memory - immunology Immunity, Innate - immunology Immunologic Memory - genetics Invertebrates - immunology Immunity, Innate - genetics Plants - immunology Vaccines - immunology Inflammation - immunology Infection - immunology Leo A B Joosten oth Eicke Latz oth Kingston H G Mills oth Gioacchino Natoli oth Hendrik G Stunnenberg oth Luke A J O'Neill oth Ramnik J Xavier oth Enthalten in Science Washington, DC : AAAS, American Assoc. for the Advancement of Science, 1883 352(2016), 6284 (DE-627)12931482X (DE-600)128410-1 (DE-576)014533189 0036-8075 nnns volume:352 year:2016 number:6284 http://dx.doi.org/10.1126/science.aaf1098 Volltext http://www.ncbi.nlm.nih.gov/pubmed/27102489 http://search.proquest.com/docview/1783557742 GBV_USEFLAG_A SYSFLAG_A GBV_OLC FID-LING SSG-OLC-PHY SSG-OLC-CHE SSG-OLC-MAT SSG-OLC-FOR SSG-OLC-SPO SSG-OLC-IBL SSG-OLC-PHA SSG-OLC-DE-84 SSG-OPC-FOR GBV_ILN_11 GBV_ILN_20 GBV_ILN_21 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_30 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_47 GBV_ILN_55 GBV_ILN_59 GBV_ILN_60 GBV_ILN_62 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_92 GBV_ILN_101 GBV_ILN_110 GBV_ILN_120 GBV_ILN_131 GBV_ILN_170 GBV_ILN_171 GBV_ILN_179 GBV_ILN_181 GBV_ILN_211 GBV_ILN_252 GBV_ILN_259 GBV_ILN_290 GBV_ILN_600 GBV_ILN_601 GBV_ILN_647 GBV_ILN_754 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2012 GBV_ILN_2015 GBV_ILN_2018 GBV_ILN_2020 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2116 GBV_ILN_2120 GBV_ILN_2121 GBV_ILN_2173 GBV_ILN_2219 GBV_ILN_2221 GBV_ILN_2279 GBV_ILN_2286 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4036 GBV_ILN_4125 GBV_ILN_4219 GBV_ILN_4251 GBV_ILN_4277 GBV_ILN_4302 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4310 GBV_ILN_4314 GBV_ILN_4317 GBV_ILN_4318 GBV_ILN_4320 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4700 AR 352 2016 6284 |
spelling |
10.1126/science.aaf1098 doi PQ20160610 (DE-627)OLC1975103874 (DE-599)GBVOLC1975103874 (PRQ)c1684-b2a624b1b5577820d4fb88e31621b33c4554976323e2a1ea7bb6181af8ed0f7a0 (KEY)0063888920160000352628400000trainedimmunityaprogramofinnateimmunememoryinhealt DE-627 ger DE-627 rakwb eng 500 DNB LING fid Mihai G Netea verfasserin aut Trained immunity: A program of innate immune memory in health and disease 2016 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier Classical immunological memory, carried out by T and B lymphocytes, ensures that we feel the ill effects of many pathogens only once. Netea et al.review how cells of the innate immune system, which lack the antigen specificity, clonality, and longevity of T cell and B cells, have some capacity to remember, too. Termed "trained immunity," the property allows macrophages, monocytes, and natural killer cells to show enhanced responsiveness when they reencounter pathogens. Epigenetic changes largely drive trained immunity, which is shorter lived and less specific than classical memory but probably still gives us a leg up during many infections. Science, this issue p. 10.1126/science.aaf1098 Host immune responses are classically divided into innate immune responses, which react rapidly and nonspecifically upon encountering a pathogen, and adaptive immune responses, which are slower to develop but are specific and build up immunological memory. The dogma that only adaptive immunity can build immunological memory has recently been challenged by studies showing that innate immune responses in plants and invertebrates (organisms lacking adaptive immune responses) can mount resistance to reinfection. Furthermore, in certain mammalian models of vaccination, protection from reinfection has been shown to occur independently of T and B lymphocytes. These observations led to the hypothesis that innate immunity can display adaptive characteristics after challenge with pathogens or their products. This de facto immunological memory has been termed "trained immunity" or "innate immune memory." In recent years, emerging evidence has shown that after infection or vaccination, prototypical innate immune cells (such as monocytes, macrophages, or natural killer cells) display long-term changes in their functional programs. These changes lead to increased responsiveness upon secondary stimulation by microbial pathogens, increased production of inflammatory mediators, and enhanced capacity to eliminate infection. Mechanistic studies have demonstrated that trained immunity is based on epigenetic reprogramming, which is broadly defined as sustained changes in transcription programs and cell physiology that do not involve permanent genetic changes, such as mutations and recombination. Histone modifications with chromatin reconfiguration have proven to be a central process for trained immunity, but other mechanisms--such as DNA methylation or modulation of microRNA and/or long noncoding RNA expression--are also expected to be involved. This leads to transcriptional programs that rewire the intracellular immune signaling of innate immune cells but also induce a shift of cellular metabolism from oxidative phosphorylation toward aerobic glycolysis, thus increasing the innate immune cells' capacity to respond to stimulation. Trained immunity programs have evolved as adaptive states that enhance fitness of the host (e.g., protective effects after infection or vaccination, or induction of mucosal tolerance toward colonizing microorganisms). Proof-of-principle experimental studies support the hypothesis that trained immunity is one of the main immunological processes that mediate the nonspecific protective effects against infections induced by vaccines, such as bacillus Calmette-Guérin or measles vaccination. However, when inappropriately activated, trained immunity programs can become maladaptive, as in postsepsis immune paralysis or autoinflammatory diseases. The discovery of trained immunity has revealed an important and previously unrecognized property of human immune responses. This advance opens the door for future research to explore trained immunity's effect on disease, for both diseases with impaired host defense, such as postsepsis immune paralysis or cancers, and autoinflammatory diseases, in which there is inappropriate activation of inflammation. These findings have considerable potential for aiding in the design of new therapeutic strategies, such as new generations of vaccines that combine classical immunological memory and trained immunity, the activation of trained immunity for the treatment of postsepsis immune paralysis or other immune deficiency states, and modulation of exaggerated inflammation in autoinflammatory diseases. Trained immunity evolved to lead to adaptive states that protect the host during microbial colonization or after infections. However, in certain situations, trained immunity may result in maladaptive states such as postsepsis immune paralysis or hyperinflammation. miRNA, microRNA. The general view that only adaptive immunity can build immunological memory has recently been challenged. In organisms lacking adaptive immunity, as well as in mammals, the innate immune system can mount resistance to reinfection, a phenomenon termed "trained immunity" or "innate immune memory." Trained immunity is orchestrated by epigenetic reprogramming, broadly defined as sustained changes in gene expression and cell physiology that do not involve permanent genetic changes such as mutations and recombination, which are essential for adaptive immunity. The discovery of trained immunity may open the door for novel vaccine approaches, new therapeutic strategies for the treatment of immune deficiency states, and modulation of exaggerated inflammation in autoinflammatory diseases. Nutzungsrecht: Copyright © 2016, American Association for the Advancement of Science. Histones - metabolism Immunologic Memory - immunology Immunity, Innate - immunology Immunologic Memory - genetics Invertebrates - immunology Immunity, Innate - genetics Plants - immunology Vaccines - immunology Inflammation - immunology Infection - immunology Leo A B Joosten oth Eicke Latz oth Kingston H G Mills oth Gioacchino Natoli oth Hendrik G Stunnenberg oth Luke A J O'Neill oth Ramnik J Xavier oth Enthalten in Science Washington, DC : AAAS, American Assoc. for the Advancement of Science, 1883 352(2016), 6284 (DE-627)12931482X (DE-600)128410-1 (DE-576)014533189 0036-8075 nnns volume:352 year:2016 number:6284 http://dx.doi.org/10.1126/science.aaf1098 Volltext http://www.ncbi.nlm.nih.gov/pubmed/27102489 http://search.proquest.com/docview/1783557742 GBV_USEFLAG_A SYSFLAG_A GBV_OLC FID-LING SSG-OLC-PHY SSG-OLC-CHE SSG-OLC-MAT SSG-OLC-FOR SSG-OLC-SPO SSG-OLC-IBL SSG-OLC-PHA SSG-OLC-DE-84 SSG-OPC-FOR GBV_ILN_11 GBV_ILN_20 GBV_ILN_21 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_30 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_47 GBV_ILN_55 GBV_ILN_59 GBV_ILN_60 GBV_ILN_62 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_92 GBV_ILN_101 GBV_ILN_110 GBV_ILN_120 GBV_ILN_131 GBV_ILN_170 GBV_ILN_171 GBV_ILN_179 GBV_ILN_181 GBV_ILN_211 GBV_ILN_252 GBV_ILN_259 GBV_ILN_290 GBV_ILN_600 GBV_ILN_601 GBV_ILN_647 GBV_ILN_754 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2012 GBV_ILN_2015 GBV_ILN_2018 GBV_ILN_2020 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2116 GBV_ILN_2120 GBV_ILN_2121 GBV_ILN_2173 GBV_ILN_2219 GBV_ILN_2221 GBV_ILN_2279 GBV_ILN_2286 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4036 GBV_ILN_4125 GBV_ILN_4219 GBV_ILN_4251 GBV_ILN_4277 GBV_ILN_4302 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4310 GBV_ILN_4314 GBV_ILN_4317 GBV_ILN_4318 GBV_ILN_4320 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4700 AR 352 2016 6284 |
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10.1126/science.aaf1098 doi PQ20160610 (DE-627)OLC1975103874 (DE-599)GBVOLC1975103874 (PRQ)c1684-b2a624b1b5577820d4fb88e31621b33c4554976323e2a1ea7bb6181af8ed0f7a0 (KEY)0063888920160000352628400000trainedimmunityaprogramofinnateimmunememoryinhealt DE-627 ger DE-627 rakwb eng 500 DNB LING fid Mihai G Netea verfasserin aut Trained immunity: A program of innate immune memory in health and disease 2016 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier Classical immunological memory, carried out by T and B lymphocytes, ensures that we feel the ill effects of many pathogens only once. Netea et al.review how cells of the innate immune system, which lack the antigen specificity, clonality, and longevity of T cell and B cells, have some capacity to remember, too. Termed "trained immunity," the property allows macrophages, monocytes, and natural killer cells to show enhanced responsiveness when they reencounter pathogens. Epigenetic changes largely drive trained immunity, which is shorter lived and less specific than classical memory but probably still gives us a leg up during many infections. Science, this issue p. 10.1126/science.aaf1098 Host immune responses are classically divided into innate immune responses, which react rapidly and nonspecifically upon encountering a pathogen, and adaptive immune responses, which are slower to develop but are specific and build up immunological memory. The dogma that only adaptive immunity can build immunological memory has recently been challenged by studies showing that innate immune responses in plants and invertebrates (organisms lacking adaptive immune responses) can mount resistance to reinfection. Furthermore, in certain mammalian models of vaccination, protection from reinfection has been shown to occur independently of T and B lymphocytes. These observations led to the hypothesis that innate immunity can display adaptive characteristics after challenge with pathogens or their products. This de facto immunological memory has been termed "trained immunity" or "innate immune memory." In recent years, emerging evidence has shown that after infection or vaccination, prototypical innate immune cells (such as monocytes, macrophages, or natural killer cells) display long-term changes in their functional programs. These changes lead to increased responsiveness upon secondary stimulation by microbial pathogens, increased production of inflammatory mediators, and enhanced capacity to eliminate infection. Mechanistic studies have demonstrated that trained immunity is based on epigenetic reprogramming, which is broadly defined as sustained changes in transcription programs and cell physiology that do not involve permanent genetic changes, such as mutations and recombination. Histone modifications with chromatin reconfiguration have proven to be a central process for trained immunity, but other mechanisms--such as DNA methylation or modulation of microRNA and/or long noncoding RNA expression--are also expected to be involved. This leads to transcriptional programs that rewire the intracellular immune signaling of innate immune cells but also induce a shift of cellular metabolism from oxidative phosphorylation toward aerobic glycolysis, thus increasing the innate immune cells' capacity to respond to stimulation. Trained immunity programs have evolved as adaptive states that enhance fitness of the host (e.g., protective effects after infection or vaccination, or induction of mucosal tolerance toward colonizing microorganisms). Proof-of-principle experimental studies support the hypothesis that trained immunity is one of the main immunological processes that mediate the nonspecific protective effects against infections induced by vaccines, such as bacillus Calmette-Guérin or measles vaccination. However, when inappropriately activated, trained immunity programs can become maladaptive, as in postsepsis immune paralysis or autoinflammatory diseases. The discovery of trained immunity has revealed an important and previously unrecognized property of human immune responses. This advance opens the door for future research to explore trained immunity's effect on disease, for both diseases with impaired host defense, such as postsepsis immune paralysis or cancers, and autoinflammatory diseases, in which there is inappropriate activation of inflammation. These findings have considerable potential for aiding in the design of new therapeutic strategies, such as new generations of vaccines that combine classical immunological memory and trained immunity, the activation of trained immunity for the treatment of postsepsis immune paralysis or other immune deficiency states, and modulation of exaggerated inflammation in autoinflammatory diseases. Trained immunity evolved to lead to adaptive states that protect the host during microbial colonization or after infections. However, in certain situations, trained immunity may result in maladaptive states such as postsepsis immune paralysis or hyperinflammation. miRNA, microRNA. The general view that only adaptive immunity can build immunological memory has recently been challenged. In organisms lacking adaptive immunity, as well as in mammals, the innate immune system can mount resistance to reinfection, a phenomenon termed "trained immunity" or "innate immune memory." Trained immunity is orchestrated by epigenetic reprogramming, broadly defined as sustained changes in gene expression and cell physiology that do not involve permanent genetic changes such as mutations and recombination, which are essential for adaptive immunity. The discovery of trained immunity may open the door for novel vaccine approaches, new therapeutic strategies for the treatment of immune deficiency states, and modulation of exaggerated inflammation in autoinflammatory diseases. Nutzungsrecht: Copyright © 2016, American Association for the Advancement of Science. Histones - metabolism Immunologic Memory - immunology Immunity, Innate - immunology Immunologic Memory - genetics Invertebrates - immunology Immunity, Innate - genetics Plants - immunology Vaccines - immunology Inflammation - immunology Infection - immunology Leo A B Joosten oth Eicke Latz oth Kingston H G Mills oth Gioacchino Natoli oth Hendrik G Stunnenberg oth Luke A J O'Neill oth Ramnik J Xavier oth Enthalten in Science Washington, DC : AAAS, American Assoc. for the Advancement of Science, 1883 352(2016), 6284 (DE-627)12931482X (DE-600)128410-1 (DE-576)014533189 0036-8075 nnns volume:352 year:2016 number:6284 http://dx.doi.org/10.1126/science.aaf1098 Volltext http://www.ncbi.nlm.nih.gov/pubmed/27102489 http://search.proquest.com/docview/1783557742 GBV_USEFLAG_A SYSFLAG_A GBV_OLC FID-LING SSG-OLC-PHY SSG-OLC-CHE SSG-OLC-MAT SSG-OLC-FOR SSG-OLC-SPO SSG-OLC-IBL SSG-OLC-PHA SSG-OLC-DE-84 SSG-OPC-FOR GBV_ILN_11 GBV_ILN_20 GBV_ILN_21 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_30 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_47 GBV_ILN_55 GBV_ILN_59 GBV_ILN_60 GBV_ILN_62 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_92 GBV_ILN_101 GBV_ILN_110 GBV_ILN_120 GBV_ILN_131 GBV_ILN_170 GBV_ILN_171 GBV_ILN_179 GBV_ILN_181 GBV_ILN_211 GBV_ILN_252 GBV_ILN_259 GBV_ILN_290 GBV_ILN_600 GBV_ILN_601 GBV_ILN_647 GBV_ILN_754 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2012 GBV_ILN_2015 GBV_ILN_2018 GBV_ILN_2020 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2116 GBV_ILN_2120 GBV_ILN_2121 GBV_ILN_2173 GBV_ILN_2219 GBV_ILN_2221 GBV_ILN_2279 GBV_ILN_2286 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4036 GBV_ILN_4125 GBV_ILN_4219 GBV_ILN_4251 GBV_ILN_4277 GBV_ILN_4302 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4310 GBV_ILN_4314 GBV_ILN_4317 GBV_ILN_4318 GBV_ILN_4320 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4700 AR 352 2016 6284 |
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10.1126/science.aaf1098 doi PQ20160610 (DE-627)OLC1975103874 (DE-599)GBVOLC1975103874 (PRQ)c1684-b2a624b1b5577820d4fb88e31621b33c4554976323e2a1ea7bb6181af8ed0f7a0 (KEY)0063888920160000352628400000trainedimmunityaprogramofinnateimmunememoryinhealt DE-627 ger DE-627 rakwb eng 500 DNB LING fid Mihai G Netea verfasserin aut Trained immunity: A program of innate immune memory in health and disease 2016 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier Classical immunological memory, carried out by T and B lymphocytes, ensures that we feel the ill effects of many pathogens only once. Netea et al.review how cells of the innate immune system, which lack the antigen specificity, clonality, and longevity of T cell and B cells, have some capacity to remember, too. Termed "trained immunity," the property allows macrophages, monocytes, and natural killer cells to show enhanced responsiveness when they reencounter pathogens. Epigenetic changes largely drive trained immunity, which is shorter lived and less specific than classical memory but probably still gives us a leg up during many infections. Science, this issue p. 10.1126/science.aaf1098 Host immune responses are classically divided into innate immune responses, which react rapidly and nonspecifically upon encountering a pathogen, and adaptive immune responses, which are slower to develop but are specific and build up immunological memory. The dogma that only adaptive immunity can build immunological memory has recently been challenged by studies showing that innate immune responses in plants and invertebrates (organisms lacking adaptive immune responses) can mount resistance to reinfection. Furthermore, in certain mammalian models of vaccination, protection from reinfection has been shown to occur independently of T and B lymphocytes. These observations led to the hypothesis that innate immunity can display adaptive characteristics after challenge with pathogens or their products. This de facto immunological memory has been termed "trained immunity" or "innate immune memory." In recent years, emerging evidence has shown that after infection or vaccination, prototypical innate immune cells (such as monocytes, macrophages, or natural killer cells) display long-term changes in their functional programs. These changes lead to increased responsiveness upon secondary stimulation by microbial pathogens, increased production of inflammatory mediators, and enhanced capacity to eliminate infection. Mechanistic studies have demonstrated that trained immunity is based on epigenetic reprogramming, which is broadly defined as sustained changes in transcription programs and cell physiology that do not involve permanent genetic changes, such as mutations and recombination. Histone modifications with chromatin reconfiguration have proven to be a central process for trained immunity, but other mechanisms--such as DNA methylation or modulation of microRNA and/or long noncoding RNA expression--are also expected to be involved. This leads to transcriptional programs that rewire the intracellular immune signaling of innate immune cells but also induce a shift of cellular metabolism from oxidative phosphorylation toward aerobic glycolysis, thus increasing the innate immune cells' capacity to respond to stimulation. Trained immunity programs have evolved as adaptive states that enhance fitness of the host (e.g., protective effects after infection or vaccination, or induction of mucosal tolerance toward colonizing microorganisms). Proof-of-principle experimental studies support the hypothesis that trained immunity is one of the main immunological processes that mediate the nonspecific protective effects against infections induced by vaccines, such as bacillus Calmette-Guérin or measles vaccination. However, when inappropriately activated, trained immunity programs can become maladaptive, as in postsepsis immune paralysis or autoinflammatory diseases. The discovery of trained immunity has revealed an important and previously unrecognized property of human immune responses. This advance opens the door for future research to explore trained immunity's effect on disease, for both diseases with impaired host defense, such as postsepsis immune paralysis or cancers, and autoinflammatory diseases, in which there is inappropriate activation of inflammation. These findings have considerable potential for aiding in the design of new therapeutic strategies, such as new generations of vaccines that combine classical immunological memory and trained immunity, the activation of trained immunity for the treatment of postsepsis immune paralysis or other immune deficiency states, and modulation of exaggerated inflammation in autoinflammatory diseases. Trained immunity evolved to lead to adaptive states that protect the host during microbial colonization or after infections. However, in certain situations, trained immunity may result in maladaptive states such as postsepsis immune paralysis or hyperinflammation. miRNA, microRNA. The general view that only adaptive immunity can build immunological memory has recently been challenged. In organisms lacking adaptive immunity, as well as in mammals, the innate immune system can mount resistance to reinfection, a phenomenon termed "trained immunity" or "innate immune memory." Trained immunity is orchestrated by epigenetic reprogramming, broadly defined as sustained changes in gene expression and cell physiology that do not involve permanent genetic changes such as mutations and recombination, which are essential for adaptive immunity. The discovery of trained immunity may open the door for novel vaccine approaches, new therapeutic strategies for the treatment of immune deficiency states, and modulation of exaggerated inflammation in autoinflammatory diseases. Nutzungsrecht: Copyright © 2016, American Association for the Advancement of Science. Histones - metabolism Immunologic Memory - immunology Immunity, Innate - immunology Immunologic Memory - genetics Invertebrates - immunology Immunity, Innate - genetics Plants - immunology Vaccines - immunology Inflammation - immunology Infection - immunology Leo A B Joosten oth Eicke Latz oth Kingston H G Mills oth Gioacchino Natoli oth Hendrik G Stunnenberg oth Luke A J O'Neill oth Ramnik J Xavier oth Enthalten in Science Washington, DC : AAAS, American Assoc. for the Advancement of Science, 1883 352(2016), 6284 (DE-627)12931482X (DE-600)128410-1 (DE-576)014533189 0036-8075 nnns volume:352 year:2016 number:6284 http://dx.doi.org/10.1126/science.aaf1098 Volltext http://www.ncbi.nlm.nih.gov/pubmed/27102489 http://search.proquest.com/docview/1783557742 GBV_USEFLAG_A SYSFLAG_A GBV_OLC FID-LING SSG-OLC-PHY SSG-OLC-CHE SSG-OLC-MAT SSG-OLC-FOR SSG-OLC-SPO SSG-OLC-IBL SSG-OLC-PHA SSG-OLC-DE-84 SSG-OPC-FOR GBV_ILN_11 GBV_ILN_20 GBV_ILN_21 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_30 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_47 GBV_ILN_55 GBV_ILN_59 GBV_ILN_60 GBV_ILN_62 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_92 GBV_ILN_101 GBV_ILN_110 GBV_ILN_120 GBV_ILN_131 GBV_ILN_170 GBV_ILN_171 GBV_ILN_179 GBV_ILN_181 GBV_ILN_211 GBV_ILN_252 GBV_ILN_259 GBV_ILN_290 GBV_ILN_600 GBV_ILN_601 GBV_ILN_647 GBV_ILN_754 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2012 GBV_ILN_2015 GBV_ILN_2018 GBV_ILN_2020 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2116 GBV_ILN_2120 GBV_ILN_2121 GBV_ILN_2173 GBV_ILN_2219 GBV_ILN_2221 GBV_ILN_2279 GBV_ILN_2286 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4036 GBV_ILN_4125 GBV_ILN_4219 GBV_ILN_4251 GBV_ILN_4277 GBV_ILN_4302 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4310 GBV_ILN_4314 GBV_ILN_4317 GBV_ILN_4318 GBV_ILN_4320 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4700 AR 352 2016 6284 |
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10.1126/science.aaf1098 doi PQ20160610 (DE-627)OLC1975103874 (DE-599)GBVOLC1975103874 (PRQ)c1684-b2a624b1b5577820d4fb88e31621b33c4554976323e2a1ea7bb6181af8ed0f7a0 (KEY)0063888920160000352628400000trainedimmunityaprogramofinnateimmunememoryinhealt DE-627 ger DE-627 rakwb eng 500 DNB LING fid Mihai G Netea verfasserin aut Trained immunity: A program of innate immune memory in health and disease 2016 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier Classical immunological memory, carried out by T and B lymphocytes, ensures that we feel the ill effects of many pathogens only once. Netea et al.review how cells of the innate immune system, which lack the antigen specificity, clonality, and longevity of T cell and B cells, have some capacity to remember, too. Termed "trained immunity," the property allows macrophages, monocytes, and natural killer cells to show enhanced responsiveness when they reencounter pathogens. Epigenetic changes largely drive trained immunity, which is shorter lived and less specific than classical memory but probably still gives us a leg up during many infections. Science, this issue p. 10.1126/science.aaf1098 Host immune responses are classically divided into innate immune responses, which react rapidly and nonspecifically upon encountering a pathogen, and adaptive immune responses, which are slower to develop but are specific and build up immunological memory. The dogma that only adaptive immunity can build immunological memory has recently been challenged by studies showing that innate immune responses in plants and invertebrates (organisms lacking adaptive immune responses) can mount resistance to reinfection. Furthermore, in certain mammalian models of vaccination, protection from reinfection has been shown to occur independently of T and B lymphocytes. These observations led to the hypothesis that innate immunity can display adaptive characteristics after challenge with pathogens or their products. This de facto immunological memory has been termed "trained immunity" or "innate immune memory." In recent years, emerging evidence has shown that after infection or vaccination, prototypical innate immune cells (such as monocytes, macrophages, or natural killer cells) display long-term changes in their functional programs. These changes lead to increased responsiveness upon secondary stimulation by microbial pathogens, increased production of inflammatory mediators, and enhanced capacity to eliminate infection. Mechanistic studies have demonstrated that trained immunity is based on epigenetic reprogramming, which is broadly defined as sustained changes in transcription programs and cell physiology that do not involve permanent genetic changes, such as mutations and recombination. Histone modifications with chromatin reconfiguration have proven to be a central process for trained immunity, but other mechanisms--such as DNA methylation or modulation of microRNA and/or long noncoding RNA expression--are also expected to be involved. This leads to transcriptional programs that rewire the intracellular immune signaling of innate immune cells but also induce a shift of cellular metabolism from oxidative phosphorylation toward aerobic glycolysis, thus increasing the innate immune cells' capacity to respond to stimulation. Trained immunity programs have evolved as adaptive states that enhance fitness of the host (e.g., protective effects after infection or vaccination, or induction of mucosal tolerance toward colonizing microorganisms). Proof-of-principle experimental studies support the hypothesis that trained immunity is one of the main immunological processes that mediate the nonspecific protective effects against infections induced by vaccines, such as bacillus Calmette-Guérin or measles vaccination. However, when inappropriately activated, trained immunity programs can become maladaptive, as in postsepsis immune paralysis or autoinflammatory diseases. The discovery of trained immunity has revealed an important and previously unrecognized property of human immune responses. This advance opens the door for future research to explore trained immunity's effect on disease, for both diseases with impaired host defense, such as postsepsis immune paralysis or cancers, and autoinflammatory diseases, in which there is inappropriate activation of inflammation. These findings have considerable potential for aiding in the design of new therapeutic strategies, such as new generations of vaccines that combine classical immunological memory and trained immunity, the activation of trained immunity for the treatment of postsepsis immune paralysis or other immune deficiency states, and modulation of exaggerated inflammation in autoinflammatory diseases. Trained immunity evolved to lead to adaptive states that protect the host during microbial colonization or after infections. However, in certain situations, trained immunity may result in maladaptive states such as postsepsis immune paralysis or hyperinflammation. miRNA, microRNA. The general view that only adaptive immunity can build immunological memory has recently been challenged. In organisms lacking adaptive immunity, as well as in mammals, the innate immune system can mount resistance to reinfection, a phenomenon termed "trained immunity" or "innate immune memory." Trained immunity is orchestrated by epigenetic reprogramming, broadly defined as sustained changes in gene expression and cell physiology that do not involve permanent genetic changes such as mutations and recombination, which are essential for adaptive immunity. The discovery of trained immunity may open the door for novel vaccine approaches, new therapeutic strategies for the treatment of immune deficiency states, and modulation of exaggerated inflammation in autoinflammatory diseases. Nutzungsrecht: Copyright © 2016, American Association for the Advancement of Science. Histones - metabolism Immunologic Memory - immunology Immunity, Innate - immunology Immunologic Memory - genetics Invertebrates - immunology Immunity, Innate - genetics Plants - immunology Vaccines - immunology Inflammation - immunology Infection - immunology Leo A B Joosten oth Eicke Latz oth Kingston H G Mills oth Gioacchino Natoli oth Hendrik G Stunnenberg oth Luke A J O'Neill oth Ramnik J Xavier oth Enthalten in Science Washington, DC : AAAS, American Assoc. for the Advancement of Science, 1883 352(2016), 6284 (DE-627)12931482X (DE-600)128410-1 (DE-576)014533189 0036-8075 nnns volume:352 year:2016 number:6284 http://dx.doi.org/10.1126/science.aaf1098 Volltext http://www.ncbi.nlm.nih.gov/pubmed/27102489 http://search.proquest.com/docview/1783557742 GBV_USEFLAG_A SYSFLAG_A GBV_OLC FID-LING SSG-OLC-PHY SSG-OLC-CHE SSG-OLC-MAT SSG-OLC-FOR SSG-OLC-SPO SSG-OLC-IBL SSG-OLC-PHA SSG-OLC-DE-84 SSG-OPC-FOR GBV_ILN_11 GBV_ILN_20 GBV_ILN_21 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_30 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_47 GBV_ILN_55 GBV_ILN_59 GBV_ILN_60 GBV_ILN_62 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_92 GBV_ILN_101 GBV_ILN_110 GBV_ILN_120 GBV_ILN_131 GBV_ILN_170 GBV_ILN_171 GBV_ILN_179 GBV_ILN_181 GBV_ILN_211 GBV_ILN_252 GBV_ILN_259 GBV_ILN_290 GBV_ILN_600 GBV_ILN_601 GBV_ILN_647 GBV_ILN_754 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2012 GBV_ILN_2015 GBV_ILN_2018 GBV_ILN_2020 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2116 GBV_ILN_2120 GBV_ILN_2121 GBV_ILN_2173 GBV_ILN_2219 GBV_ILN_2221 GBV_ILN_2279 GBV_ILN_2286 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4036 GBV_ILN_4125 GBV_ILN_4219 GBV_ILN_4251 GBV_ILN_4277 GBV_ILN_4302 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4310 GBV_ILN_4314 GBV_ILN_4317 GBV_ILN_4318 GBV_ILN_4320 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4700 AR 352 2016 6284 |
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Histones - metabolism Immunologic Memory - immunology Immunity, Innate - immunology Immunologic Memory - genetics Invertebrates - immunology Immunity, Innate - genetics Plants - immunology Vaccines - immunology Inflammation - immunology Infection - immunology |
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Mihai G Netea @@aut@@ Leo A B Joosten @@oth@@ Eicke Latz @@oth@@ Kingston H G Mills @@oth@@ Gioacchino Natoli @@oth@@ Hendrik G Stunnenberg @@oth@@ Luke A J O'Neill @@oth@@ Ramnik J Xavier @@oth@@ |
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Netea et al.review how cells of the innate immune system, which lack the antigen specificity, clonality, and longevity of T cell and B cells, have some capacity to remember, too. Termed "trained immunity," the property allows macrophages, monocytes, and natural killer cells to show enhanced responsiveness when they reencounter pathogens. Epigenetic changes largely drive trained immunity, which is shorter lived and less specific than classical memory but probably still gives us a leg up during many infections. Science, this issue p. 10.1126/science.aaf1098 Host immune responses are classically divided into innate immune responses, which react rapidly and nonspecifically upon encountering a pathogen, and adaptive immune responses, which are slower to develop but are specific and build up immunological memory. The dogma that only adaptive immunity can build immunological memory has recently been challenged by studies showing that innate immune responses in plants and invertebrates (organisms lacking adaptive immune responses) can mount resistance to reinfection. Furthermore, in certain mammalian models of vaccination, protection from reinfection has been shown to occur independently of T and B lymphocytes. These observations led to the hypothesis that innate immunity can display adaptive characteristics after challenge with pathogens or their products. This de facto immunological memory has been termed "trained immunity" or "innate immune memory." In recent years, emerging evidence has shown that after infection or vaccination, prototypical innate immune cells (such as monocytes, macrophages, or natural killer cells) display long-term changes in their functional programs. These changes lead to increased responsiveness upon secondary stimulation by microbial pathogens, increased production of inflammatory mediators, and enhanced capacity to eliminate infection. Mechanistic studies have demonstrated that trained immunity is based on epigenetic reprogramming, which is broadly defined as sustained changes in transcription programs and cell physiology that do not involve permanent genetic changes, such as mutations and recombination. Histone modifications with chromatin reconfiguration have proven to be a central process for trained immunity, but other mechanisms--such as DNA methylation or modulation of microRNA and/or long noncoding RNA expression--are also expected to be involved. This leads to transcriptional programs that rewire the intracellular immune signaling of innate immune cells but also induce a shift of cellular metabolism from oxidative phosphorylation toward aerobic glycolysis, thus increasing the innate immune cells' capacity to respond to stimulation. Trained immunity programs have evolved as adaptive states that enhance fitness of the host (e.g., protective effects after infection or vaccination, or induction of mucosal tolerance toward colonizing microorganisms). Proof-of-principle experimental studies support the hypothesis that trained immunity is one of the main immunological processes that mediate the nonspecific protective effects against infections induced by vaccines, such as bacillus Calmette-Guérin or measles vaccination. However, when inappropriately activated, trained immunity programs can become maladaptive, as in postsepsis immune paralysis or autoinflammatory diseases. The discovery of trained immunity has revealed an important and previously unrecognized property of human immune responses. This advance opens the door for future research to explore trained immunity's effect on disease, for both diseases with impaired host defense, such as postsepsis immune paralysis or cancers, and autoinflammatory diseases, in which there is inappropriate activation of inflammation. These findings have considerable potential for aiding in the design of new therapeutic strategies, such as new generations of vaccines that combine classical immunological memory and trained immunity, the activation of trained immunity for the treatment of postsepsis immune paralysis or other immune deficiency states, and modulation of exaggerated inflammation in autoinflammatory diseases. Trained immunity evolved to lead to adaptive states that protect the host during microbial colonization or after infections. 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Mihai G Netea |
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Trained immunity: A program of innate immune memory in health and disease |
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trained immunity: a program of innate immune memory in health and disease |
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Trained immunity: A program of innate immune memory in health and disease |
abstract |
Classical immunological memory, carried out by T and B lymphocytes, ensures that we feel the ill effects of many pathogens only once. Netea et al.review how cells of the innate immune system, which lack the antigen specificity, clonality, and longevity of T cell and B cells, have some capacity to remember, too. Termed "trained immunity," the property allows macrophages, monocytes, and natural killer cells to show enhanced responsiveness when they reencounter pathogens. Epigenetic changes largely drive trained immunity, which is shorter lived and less specific than classical memory but probably still gives us a leg up during many infections. Science, this issue p. 10.1126/science.aaf1098 Host immune responses are classically divided into innate immune responses, which react rapidly and nonspecifically upon encountering a pathogen, and adaptive immune responses, which are slower to develop but are specific and build up immunological memory. The dogma that only adaptive immunity can build immunological memory has recently been challenged by studies showing that innate immune responses in plants and invertebrates (organisms lacking adaptive immune responses) can mount resistance to reinfection. Furthermore, in certain mammalian models of vaccination, protection from reinfection has been shown to occur independently of T and B lymphocytes. These observations led to the hypothesis that innate immunity can display adaptive characteristics after challenge with pathogens or their products. This de facto immunological memory has been termed "trained immunity" or "innate immune memory." In recent years, emerging evidence has shown that after infection or vaccination, prototypical innate immune cells (such as monocytes, macrophages, or natural killer cells) display long-term changes in their functional programs. These changes lead to increased responsiveness upon secondary stimulation by microbial pathogens, increased production of inflammatory mediators, and enhanced capacity to eliminate infection. Mechanistic studies have demonstrated that trained immunity is based on epigenetic reprogramming, which is broadly defined as sustained changes in transcription programs and cell physiology that do not involve permanent genetic changes, such as mutations and recombination. Histone modifications with chromatin reconfiguration have proven to be a central process for trained immunity, but other mechanisms--such as DNA methylation or modulation of microRNA and/or long noncoding RNA expression--are also expected to be involved. This leads to transcriptional programs that rewire the intracellular immune signaling of innate immune cells but also induce a shift of cellular metabolism from oxidative phosphorylation toward aerobic glycolysis, thus increasing the innate immune cells' capacity to respond to stimulation. Trained immunity programs have evolved as adaptive states that enhance fitness of the host (e.g., protective effects after infection or vaccination, or induction of mucosal tolerance toward colonizing microorganisms). Proof-of-principle experimental studies support the hypothesis that trained immunity is one of the main immunological processes that mediate the nonspecific protective effects against infections induced by vaccines, such as bacillus Calmette-Guérin or measles vaccination. However, when inappropriately activated, trained immunity programs can become maladaptive, as in postsepsis immune paralysis or autoinflammatory diseases. The discovery of trained immunity has revealed an important and previously unrecognized property of human immune responses. This advance opens the door for future research to explore trained immunity's effect on disease, for both diseases with impaired host defense, such as postsepsis immune paralysis or cancers, and autoinflammatory diseases, in which there is inappropriate activation of inflammation. These findings have considerable potential for aiding in the design of new therapeutic strategies, such as new generations of vaccines that combine classical immunological memory and trained immunity, the activation of trained immunity for the treatment of postsepsis immune paralysis or other immune deficiency states, and modulation of exaggerated inflammation in autoinflammatory diseases. Trained immunity evolved to lead to adaptive states that protect the host during microbial colonization or after infections. However, in certain situations, trained immunity may result in maladaptive states such as postsepsis immune paralysis or hyperinflammation. miRNA, microRNA. The general view that only adaptive immunity can build immunological memory has recently been challenged. In organisms lacking adaptive immunity, as well as in mammals, the innate immune system can mount resistance to reinfection, a phenomenon termed "trained immunity" or "innate immune memory." Trained immunity is orchestrated by epigenetic reprogramming, broadly defined as sustained changes in gene expression and cell physiology that do not involve permanent genetic changes such as mutations and recombination, which are essential for adaptive immunity. The discovery of trained immunity may open the door for novel vaccine approaches, new therapeutic strategies for the treatment of immune deficiency states, and modulation of exaggerated inflammation in autoinflammatory diseases. |
abstractGer |
Classical immunological memory, carried out by T and B lymphocytes, ensures that we feel the ill effects of many pathogens only once. Netea et al.review how cells of the innate immune system, which lack the antigen specificity, clonality, and longevity of T cell and B cells, have some capacity to remember, too. Termed "trained immunity," the property allows macrophages, monocytes, and natural killer cells to show enhanced responsiveness when they reencounter pathogens. Epigenetic changes largely drive trained immunity, which is shorter lived and less specific than classical memory but probably still gives us a leg up during many infections. Science, this issue p. 10.1126/science.aaf1098 Host immune responses are classically divided into innate immune responses, which react rapidly and nonspecifically upon encountering a pathogen, and adaptive immune responses, which are slower to develop but are specific and build up immunological memory. The dogma that only adaptive immunity can build immunological memory has recently been challenged by studies showing that innate immune responses in plants and invertebrates (organisms lacking adaptive immune responses) can mount resistance to reinfection. Furthermore, in certain mammalian models of vaccination, protection from reinfection has been shown to occur independently of T and B lymphocytes. These observations led to the hypothesis that innate immunity can display adaptive characteristics after challenge with pathogens or their products. This de facto immunological memory has been termed "trained immunity" or "innate immune memory." In recent years, emerging evidence has shown that after infection or vaccination, prototypical innate immune cells (such as monocytes, macrophages, or natural killer cells) display long-term changes in their functional programs. These changes lead to increased responsiveness upon secondary stimulation by microbial pathogens, increased production of inflammatory mediators, and enhanced capacity to eliminate infection. Mechanistic studies have demonstrated that trained immunity is based on epigenetic reprogramming, which is broadly defined as sustained changes in transcription programs and cell physiology that do not involve permanent genetic changes, such as mutations and recombination. Histone modifications with chromatin reconfiguration have proven to be a central process for trained immunity, but other mechanisms--such as DNA methylation or modulation of microRNA and/or long noncoding RNA expression--are also expected to be involved. This leads to transcriptional programs that rewire the intracellular immune signaling of innate immune cells but also induce a shift of cellular metabolism from oxidative phosphorylation toward aerobic glycolysis, thus increasing the innate immune cells' capacity to respond to stimulation. Trained immunity programs have evolved as adaptive states that enhance fitness of the host (e.g., protective effects after infection or vaccination, or induction of mucosal tolerance toward colonizing microorganisms). Proof-of-principle experimental studies support the hypothesis that trained immunity is one of the main immunological processes that mediate the nonspecific protective effects against infections induced by vaccines, such as bacillus Calmette-Guérin or measles vaccination. However, when inappropriately activated, trained immunity programs can become maladaptive, as in postsepsis immune paralysis or autoinflammatory diseases. The discovery of trained immunity has revealed an important and previously unrecognized property of human immune responses. This advance opens the door for future research to explore trained immunity's effect on disease, for both diseases with impaired host defense, such as postsepsis immune paralysis or cancers, and autoinflammatory diseases, in which there is inappropriate activation of inflammation. These findings have considerable potential for aiding in the design of new therapeutic strategies, such as new generations of vaccines that combine classical immunological memory and trained immunity, the activation of trained immunity for the treatment of postsepsis immune paralysis or other immune deficiency states, and modulation of exaggerated inflammation in autoinflammatory diseases. Trained immunity evolved to lead to adaptive states that protect the host during microbial colonization or after infections. However, in certain situations, trained immunity may result in maladaptive states such as postsepsis immune paralysis or hyperinflammation. miRNA, microRNA. The general view that only adaptive immunity can build immunological memory has recently been challenged. In organisms lacking adaptive immunity, as well as in mammals, the innate immune system can mount resistance to reinfection, a phenomenon termed "trained immunity" or "innate immune memory." Trained immunity is orchestrated by epigenetic reprogramming, broadly defined as sustained changes in gene expression and cell physiology that do not involve permanent genetic changes such as mutations and recombination, which are essential for adaptive immunity. The discovery of trained immunity may open the door for novel vaccine approaches, new therapeutic strategies for the treatment of immune deficiency states, and modulation of exaggerated inflammation in autoinflammatory diseases. |
abstract_unstemmed |
Classical immunological memory, carried out by T and B lymphocytes, ensures that we feel the ill effects of many pathogens only once. Netea et al.review how cells of the innate immune system, which lack the antigen specificity, clonality, and longevity of T cell and B cells, have some capacity to remember, too. Termed "trained immunity," the property allows macrophages, monocytes, and natural killer cells to show enhanced responsiveness when they reencounter pathogens. Epigenetic changes largely drive trained immunity, which is shorter lived and less specific than classical memory but probably still gives us a leg up during many infections. Science, this issue p. 10.1126/science.aaf1098 Host immune responses are classically divided into innate immune responses, which react rapidly and nonspecifically upon encountering a pathogen, and adaptive immune responses, which are slower to develop but are specific and build up immunological memory. The dogma that only adaptive immunity can build immunological memory has recently been challenged by studies showing that innate immune responses in plants and invertebrates (organisms lacking adaptive immune responses) can mount resistance to reinfection. Furthermore, in certain mammalian models of vaccination, protection from reinfection has been shown to occur independently of T and B lymphocytes. These observations led to the hypothesis that innate immunity can display adaptive characteristics after challenge with pathogens or their products. This de facto immunological memory has been termed "trained immunity" or "innate immune memory." In recent years, emerging evidence has shown that after infection or vaccination, prototypical innate immune cells (such as monocytes, macrophages, or natural killer cells) display long-term changes in their functional programs. These changes lead to increased responsiveness upon secondary stimulation by microbial pathogens, increased production of inflammatory mediators, and enhanced capacity to eliminate infection. Mechanistic studies have demonstrated that trained immunity is based on epigenetic reprogramming, which is broadly defined as sustained changes in transcription programs and cell physiology that do not involve permanent genetic changes, such as mutations and recombination. Histone modifications with chromatin reconfiguration have proven to be a central process for trained immunity, but other mechanisms--such as DNA methylation or modulation of microRNA and/or long noncoding RNA expression--are also expected to be involved. This leads to transcriptional programs that rewire the intracellular immune signaling of innate immune cells but also induce a shift of cellular metabolism from oxidative phosphorylation toward aerobic glycolysis, thus increasing the innate immune cells' capacity to respond to stimulation. Trained immunity programs have evolved as adaptive states that enhance fitness of the host (e.g., protective effects after infection or vaccination, or induction of mucosal tolerance toward colonizing microorganisms). Proof-of-principle experimental studies support the hypothesis that trained immunity is one of the main immunological processes that mediate the nonspecific protective effects against infections induced by vaccines, such as bacillus Calmette-Guérin or measles vaccination. However, when inappropriately activated, trained immunity programs can become maladaptive, as in postsepsis immune paralysis or autoinflammatory diseases. The discovery of trained immunity has revealed an important and previously unrecognized property of human immune responses. This advance opens the door for future research to explore trained immunity's effect on disease, for both diseases with impaired host defense, such as postsepsis immune paralysis or cancers, and autoinflammatory diseases, in which there is inappropriate activation of inflammation. These findings have considerable potential for aiding in the design of new therapeutic strategies, such as new generations of vaccines that combine classical immunological memory and trained immunity, the activation of trained immunity for the treatment of postsepsis immune paralysis or other immune deficiency states, and modulation of exaggerated inflammation in autoinflammatory diseases. Trained immunity evolved to lead to adaptive states that protect the host during microbial colonization or after infections. However, in certain situations, trained immunity may result in maladaptive states such as postsepsis immune paralysis or hyperinflammation. miRNA, microRNA. The general view that only adaptive immunity can build immunological memory has recently been challenged. In organisms lacking adaptive immunity, as well as in mammals, the innate immune system can mount resistance to reinfection, a phenomenon termed "trained immunity" or "innate immune memory." Trained immunity is orchestrated by epigenetic reprogramming, broadly defined as sustained changes in gene expression and cell physiology that do not involve permanent genetic changes such as mutations and recombination, which are essential for adaptive immunity. The discovery of trained immunity may open the door for novel vaccine approaches, new therapeutic strategies for the treatment of immune deficiency states, and modulation of exaggerated inflammation in autoinflammatory diseases. |
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title_short |
Trained immunity: A program of innate immune memory in health and disease |
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http://dx.doi.org/10.1126/science.aaf1098 http://www.ncbi.nlm.nih.gov/pubmed/27102489 http://search.proquest.com/docview/1783557742 |
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Leo A B Joosten Eicke Latz Kingston H G Mills Gioacchino Natoli Hendrik G Stunnenberg Luke A J O'Neill Ramnik J Xavier |
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Leo A B Joosten Eicke Latz Kingston H G Mills Gioacchino Natoli Hendrik G Stunnenberg Luke A J O'Neill Ramnik J Xavier |
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The dogma that only adaptive immunity can build immunological memory has recently been challenged by studies showing that innate immune responses in plants and invertebrates (organisms lacking adaptive immune responses) can mount resistance to reinfection. Furthermore, in certain mammalian models of vaccination, protection from reinfection has been shown to occur independently of T and B lymphocytes. These observations led to the hypothesis that innate immunity can display adaptive characteristics after challenge with pathogens or their products. This de facto immunological memory has been termed "trained immunity" or "innate immune memory." In recent years, emerging evidence has shown that after infection or vaccination, prototypical innate immune cells (such as monocytes, macrophages, or natural killer cells) display long-term changes in their functional programs. 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