Helicobacter pylori, T cells and cytokines: the “dangerous liaisons”
Helicobacter pylori infection is the major cause of gastroduodenal pathologies, but only a minority of infected patients develop chronic and life threatening diseases, as peptic ulcer, gastric cancer, B-cell lymphoma, or autoimmune gastritis. The type of host immune response against H. pylori is cru...
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| Autor*in: |
D'Elios, Mario Milco [verfasserIn] Amedei, Amedeo [verfasserIn] Benagiano, Marisa [verfasserIn] |
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| Format: |
E-Artikel |
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| Erschienen: |
Oxford, UK: Blackwell Publishing Ltd ; 2005 |
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| Schlagwörter: |
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| Umfang: |
Online-Ressource |
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| Reproduktion: |
2006 ; Blackwell Publishing Journal Backfiles 1879-2005 |
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| Übergeordnetes Werk: |
In: FEMS immunology and medical microbiology - Federation of European Microbiological Societies ; GKD-ID: 114439X, Oxford [u.a.] : Wiley-Blackwell, 1993, 44(2005), 2, Seite 0 |
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volume:44 ; year:2005 ; number:2 ; pages:0 |
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| DOI / URN: |
10.1016/j.femsim.2004.10.013 |
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| 520 | |a Helicobacter pylori infection is the major cause of gastroduodenal pathologies, but only a minority of infected patients develop chronic and life threatening diseases, as peptic ulcer, gastric cancer, B-cell lymphoma, or autoimmune gastritis. The type of host immune response against H. pylori is crucial for the outcome of the infection. A predominant H. pylori-specific Th1 response, characterized by high IFN-γ, TNF-α, and IL-12 production associates with peptic ulcer, whereas combined secretion of both Th1 and Th2 cytokines are present in uncomplicated gastritis. Gastric T cells from MALT lymphoma exhibit abnormal help for autologous B-cell proliferation and reduced perforin- and Fas–Fas ligand-mediated killing of B cells. In H. pylori-infected patients with autoimmune gastritis cytolytic T cells infiltrating the gastric mucosa cross-recognize different epitopes of H. pylori proteins and H+K+ ATPase autoantigen. These data suggest that peptic ulcer can be regarded as a Th1-driven immunopathological response to some H. pylori antigens, whereas deregulated and exhaustive H. pylori-induced T cell-dependent B-cell activation can support the onset of low-grade B-cell lymphoma. Alternatively, H. pylori infection may lead in some individuals to gastric autoimmunity via molecular mimicry. | ||
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10.1016/j.femsim.2004.10.013 doi (DE-627)NLEJ242922880 DE-627 ger DE-627 rakwb D'Elios, Mario Milco verfasserin aut Helicobacter pylori, T cells and cytokines: the “dangerous liaisons” Oxford, UK Blackwell Publishing Ltd 2005 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Helicobacter pylori infection is the major cause of gastroduodenal pathologies, but only a minority of infected patients develop chronic and life threatening diseases, as peptic ulcer, gastric cancer, B-cell lymphoma, or autoimmune gastritis. The type of host immune response against H. pylori is crucial for the outcome of the infection. A predominant H. pylori-specific Th1 response, characterized by high IFN-γ, TNF-α, and IL-12 production associates with peptic ulcer, whereas combined secretion of both Th1 and Th2 cytokines are present in uncomplicated gastritis. Gastric T cells from MALT lymphoma exhibit abnormal help for autologous B-cell proliferation and reduced perforin- and Fas–Fas ligand-mediated killing of B cells. In H. pylori-infected patients with autoimmune gastritis cytolytic T cells infiltrating the gastric mucosa cross-recognize different epitopes of H. pylori proteins and H+K+ ATPase autoantigen. These data suggest that peptic ulcer can be regarded as a Th1-driven immunopathological response to some H. pylori antigens, whereas deregulated and exhaustive H. pylori-induced T cell-dependent B-cell activation can support the onset of low-grade B-cell lymphoma. Alternatively, H. pylori infection may lead in some individuals to gastric autoimmunity via molecular mimicry. 2006 Blackwell Publishing Journal Backfiles 1879-2005 |2006|||||||||| Mucosal immunity Amedei, Amedeo verfasserin aut Benagiano, Marisa verfasserin aut Azzurri, Annalisa oth Prete, Gianfranco oth In Federation of European Microbiological Societies ; GKD-ID: 114439X FEMS immunology and medical microbiology Oxford [u.a.] : Wiley-Blackwell, 1993 44(2005), 2, Seite 0 Online-Ressource (DE-627)NLEJ243926014 (DE-600)1500464-8 1574-695X nnns volume:44 year:2005 number:2 pages:0 http://dx.doi.org/10.1016/j.femsim.2004.10.013 text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 44 2005 2 0 |
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10.1016/j.femsim.2004.10.013 doi (DE-627)NLEJ242922880 DE-627 ger DE-627 rakwb D'Elios, Mario Milco verfasserin aut Helicobacter pylori, T cells and cytokines: the “dangerous liaisons” Oxford, UK Blackwell Publishing Ltd 2005 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Helicobacter pylori infection is the major cause of gastroduodenal pathologies, but only a minority of infected patients develop chronic and life threatening diseases, as peptic ulcer, gastric cancer, B-cell lymphoma, or autoimmune gastritis. The type of host immune response against H. pylori is crucial for the outcome of the infection. A predominant H. pylori-specific Th1 response, characterized by high IFN-γ, TNF-α, and IL-12 production associates with peptic ulcer, whereas combined secretion of both Th1 and Th2 cytokines are present in uncomplicated gastritis. Gastric T cells from MALT lymphoma exhibit abnormal help for autologous B-cell proliferation and reduced perforin- and Fas–Fas ligand-mediated killing of B cells. In H. pylori-infected patients with autoimmune gastritis cytolytic T cells infiltrating the gastric mucosa cross-recognize different epitopes of H. pylori proteins and H+K+ ATPase autoantigen. These data suggest that peptic ulcer can be regarded as a Th1-driven immunopathological response to some H. pylori antigens, whereas deregulated and exhaustive H. pylori-induced T cell-dependent B-cell activation can support the onset of low-grade B-cell lymphoma. Alternatively, H. pylori infection may lead in some individuals to gastric autoimmunity via molecular mimicry. 2006 Blackwell Publishing Journal Backfiles 1879-2005 |2006|||||||||| Mucosal immunity Amedei, Amedeo verfasserin aut Benagiano, Marisa verfasserin aut Azzurri, Annalisa oth Prete, Gianfranco oth In Federation of European Microbiological Societies ; GKD-ID: 114439X FEMS immunology and medical microbiology Oxford [u.a.] : Wiley-Blackwell, 1993 44(2005), 2, Seite 0 Online-Ressource (DE-627)NLEJ243926014 (DE-600)1500464-8 1574-695X nnns volume:44 year:2005 number:2 pages:0 http://dx.doi.org/10.1016/j.femsim.2004.10.013 text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 44 2005 2 0 |
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10.1016/j.femsim.2004.10.013 doi (DE-627)NLEJ242922880 DE-627 ger DE-627 rakwb D'Elios, Mario Milco verfasserin aut Helicobacter pylori, T cells and cytokines: the “dangerous liaisons” Oxford, UK Blackwell Publishing Ltd 2005 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Helicobacter pylori infection is the major cause of gastroduodenal pathologies, but only a minority of infected patients develop chronic and life threatening diseases, as peptic ulcer, gastric cancer, B-cell lymphoma, or autoimmune gastritis. The type of host immune response against H. pylori is crucial for the outcome of the infection. A predominant H. pylori-specific Th1 response, characterized by high IFN-γ, TNF-α, and IL-12 production associates with peptic ulcer, whereas combined secretion of both Th1 and Th2 cytokines are present in uncomplicated gastritis. Gastric T cells from MALT lymphoma exhibit abnormal help for autologous B-cell proliferation and reduced perforin- and Fas–Fas ligand-mediated killing of B cells. In H. pylori-infected patients with autoimmune gastritis cytolytic T cells infiltrating the gastric mucosa cross-recognize different epitopes of H. pylori proteins and H+K+ ATPase autoantigen. These data suggest that peptic ulcer can be regarded as a Th1-driven immunopathological response to some H. pylori antigens, whereas deregulated and exhaustive H. pylori-induced T cell-dependent B-cell activation can support the onset of low-grade B-cell lymphoma. Alternatively, H. pylori infection may lead in some individuals to gastric autoimmunity via molecular mimicry. 2006 Blackwell Publishing Journal Backfiles 1879-2005 |2006|||||||||| Mucosal immunity Amedei, Amedeo verfasserin aut Benagiano, Marisa verfasserin aut Azzurri, Annalisa oth Prete, Gianfranco oth In Federation of European Microbiological Societies ; GKD-ID: 114439X FEMS immunology and medical microbiology Oxford [u.a.] : Wiley-Blackwell, 1993 44(2005), 2, Seite 0 Online-Ressource (DE-627)NLEJ243926014 (DE-600)1500464-8 1574-695X nnns volume:44 year:2005 number:2 pages:0 http://dx.doi.org/10.1016/j.femsim.2004.10.013 text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 44 2005 2 0 |
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10.1016/j.femsim.2004.10.013 doi (DE-627)NLEJ242922880 DE-627 ger DE-627 rakwb D'Elios, Mario Milco verfasserin aut Helicobacter pylori, T cells and cytokines: the “dangerous liaisons” Oxford, UK Blackwell Publishing Ltd 2005 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Helicobacter pylori infection is the major cause of gastroduodenal pathologies, but only a minority of infected patients develop chronic and life threatening diseases, as peptic ulcer, gastric cancer, B-cell lymphoma, or autoimmune gastritis. The type of host immune response against H. pylori is crucial for the outcome of the infection. A predominant H. pylori-specific Th1 response, characterized by high IFN-γ, TNF-α, and IL-12 production associates with peptic ulcer, whereas combined secretion of both Th1 and Th2 cytokines are present in uncomplicated gastritis. Gastric T cells from MALT lymphoma exhibit abnormal help for autologous B-cell proliferation and reduced perforin- and Fas–Fas ligand-mediated killing of B cells. In H. pylori-infected patients with autoimmune gastritis cytolytic T cells infiltrating the gastric mucosa cross-recognize different epitopes of H. pylori proteins and H+K+ ATPase autoantigen. These data suggest that peptic ulcer can be regarded as a Th1-driven immunopathological response to some H. pylori antigens, whereas deregulated and exhaustive H. pylori-induced T cell-dependent B-cell activation can support the onset of low-grade B-cell lymphoma. Alternatively, H. pylori infection may lead in some individuals to gastric autoimmunity via molecular mimicry. 2006 Blackwell Publishing Journal Backfiles 1879-2005 |2006|||||||||| Mucosal immunity Amedei, Amedeo verfasserin aut Benagiano, Marisa verfasserin aut Azzurri, Annalisa oth Prete, Gianfranco oth In Federation of European Microbiological Societies ; GKD-ID: 114439X FEMS immunology and medical microbiology Oxford [u.a.] : Wiley-Blackwell, 1993 44(2005), 2, Seite 0 Online-Ressource (DE-627)NLEJ243926014 (DE-600)1500464-8 1574-695X nnns volume:44 year:2005 number:2 pages:0 http://dx.doi.org/10.1016/j.femsim.2004.10.013 text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 44 2005 2 0 |
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10.1016/j.femsim.2004.10.013 doi (DE-627)NLEJ242922880 DE-627 ger DE-627 rakwb D'Elios, Mario Milco verfasserin aut Helicobacter pylori, T cells and cytokines: the “dangerous liaisons” Oxford, UK Blackwell Publishing Ltd 2005 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Helicobacter pylori infection is the major cause of gastroduodenal pathologies, but only a minority of infected patients develop chronic and life threatening diseases, as peptic ulcer, gastric cancer, B-cell lymphoma, or autoimmune gastritis. The type of host immune response against H. pylori is crucial for the outcome of the infection. A predominant H. pylori-specific Th1 response, characterized by high IFN-γ, TNF-α, and IL-12 production associates with peptic ulcer, whereas combined secretion of both Th1 and Th2 cytokines are present in uncomplicated gastritis. Gastric T cells from MALT lymphoma exhibit abnormal help for autologous B-cell proliferation and reduced perforin- and Fas–Fas ligand-mediated killing of B cells. In H. pylori-infected patients with autoimmune gastritis cytolytic T cells infiltrating the gastric mucosa cross-recognize different epitopes of H. pylori proteins and H+K+ ATPase autoantigen. These data suggest that peptic ulcer can be regarded as a Th1-driven immunopathological response to some H. pylori antigens, whereas deregulated and exhaustive H. pylori-induced T cell-dependent B-cell activation can support the onset of low-grade B-cell lymphoma. Alternatively, H. pylori infection may lead in some individuals to gastric autoimmunity via molecular mimicry. 2006 Blackwell Publishing Journal Backfiles 1879-2005 |2006|||||||||| Mucosal immunity Amedei, Amedeo verfasserin aut Benagiano, Marisa verfasserin aut Azzurri, Annalisa oth Prete, Gianfranco oth In Federation of European Microbiological Societies ; GKD-ID: 114439X FEMS immunology and medical microbiology Oxford [u.a.] : Wiley-Blackwell, 1993 44(2005), 2, Seite 0 Online-Ressource (DE-627)NLEJ243926014 (DE-600)1500464-8 1574-695X nnns volume:44 year:2005 number:2 pages:0 http://dx.doi.org/10.1016/j.femsim.2004.10.013 text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 44 2005 2 0 |
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Helicobacter pylori, T cells and cytokines: the “dangerous liaisons” |
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Helicobacter pylori infection is the major cause of gastroduodenal pathologies, but only a minority of infected patients develop chronic and life threatening diseases, as peptic ulcer, gastric cancer, B-cell lymphoma, or autoimmune gastritis. The type of host immune response against H. pylori is crucial for the outcome of the infection. A predominant H. pylori-specific Th1 response, characterized by high IFN-γ, TNF-α, and IL-12 production associates with peptic ulcer, whereas combined secretion of both Th1 and Th2 cytokines are present in uncomplicated gastritis. Gastric T cells from MALT lymphoma exhibit abnormal help for autologous B-cell proliferation and reduced perforin- and Fas–Fas ligand-mediated killing of B cells. In H. pylori-infected patients with autoimmune gastritis cytolytic T cells infiltrating the gastric mucosa cross-recognize different epitopes of H. pylori proteins and H+K+ ATPase autoantigen. These data suggest that peptic ulcer can be regarded as a Th1-driven immunopathological response to some H. pylori antigens, whereas deregulated and exhaustive H. pylori-induced T cell-dependent B-cell activation can support the onset of low-grade B-cell lymphoma. Alternatively, H. pylori infection may lead in some individuals to gastric autoimmunity via molecular mimicry. |
| abstractGer |
Helicobacter pylori infection is the major cause of gastroduodenal pathologies, but only a minority of infected patients develop chronic and life threatening diseases, as peptic ulcer, gastric cancer, B-cell lymphoma, or autoimmune gastritis. The type of host immune response against H. pylori is crucial for the outcome of the infection. A predominant H. pylori-specific Th1 response, characterized by high IFN-γ, TNF-α, and IL-12 production associates with peptic ulcer, whereas combined secretion of both Th1 and Th2 cytokines are present in uncomplicated gastritis. Gastric T cells from MALT lymphoma exhibit abnormal help for autologous B-cell proliferation and reduced perforin- and Fas–Fas ligand-mediated killing of B cells. In H. pylori-infected patients with autoimmune gastritis cytolytic T cells infiltrating the gastric mucosa cross-recognize different epitopes of H. pylori proteins and H+K+ ATPase autoantigen. These data suggest that peptic ulcer can be regarded as a Th1-driven immunopathological response to some H. pylori antigens, whereas deregulated and exhaustive H. pylori-induced T cell-dependent B-cell activation can support the onset of low-grade B-cell lymphoma. Alternatively, H. pylori infection may lead in some individuals to gastric autoimmunity via molecular mimicry. |
| abstract_unstemmed |
Helicobacter pylori infection is the major cause of gastroduodenal pathologies, but only a minority of infected patients develop chronic and life threatening diseases, as peptic ulcer, gastric cancer, B-cell lymphoma, or autoimmune gastritis. The type of host immune response against H. pylori is crucial for the outcome of the infection. A predominant H. pylori-specific Th1 response, characterized by high IFN-γ, TNF-α, and IL-12 production associates with peptic ulcer, whereas combined secretion of both Th1 and Th2 cytokines are present in uncomplicated gastritis. Gastric T cells from MALT lymphoma exhibit abnormal help for autologous B-cell proliferation and reduced perforin- and Fas–Fas ligand-mediated killing of B cells. In H. pylori-infected patients with autoimmune gastritis cytolytic T cells infiltrating the gastric mucosa cross-recognize different epitopes of H. pylori proteins and H+K+ ATPase autoantigen. These data suggest that peptic ulcer can be regarded as a Th1-driven immunopathological response to some H. pylori antigens, whereas deregulated and exhaustive H. pylori-induced T cell-dependent B-cell activation can support the onset of low-grade B-cell lymphoma. Alternatively, H. pylori infection may lead in some individuals to gastric autoimmunity via molecular mimicry. |
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Amedei, Amedeo Benagiano, Marisa Azzurri, Annalisa Prete, Gianfranco |
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