Innate Immune Responses in Transplant Immunity
Purpose of Review Despite a significant decrease in the rate of acute rejection, long-term solid organ allotransplant success is limited by chronic rejection. Transplant research has historically focused on adaptive immune responses. However, there is a growing appreciation that the innate immune sy...
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| Autor*in: |
Ladowski, Joseph M. [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2023 |
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| Schlagwörter: |
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| Anmerkung: |
© The Author(s), under exclusive licence to Springer Nature Switzerland AG 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. |
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| Übergeordnetes Werk: |
Enthalten in: Current transplantation reports - Cham : Springer Internat. Publ., 2014, 10(2023), 4 vom: 27. Nov., Seite 237-244 |
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| Übergeordnetes Werk: |
volume:10 ; year:2023 ; number:4 ; day:27 ; month:11 ; pages:237-244 |
| Links: |
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| DOI / URN: |
10.1007/s40472-023-00422-4 |
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| Katalog-ID: |
SPR054173175 |
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| 520 | |a Purpose of Review Despite a significant decrease in the rate of acute rejection, long-term solid organ allotransplant success is limited by chronic rejection. Transplant research has historically focused on adaptive immune responses. However, there is a growing appreciation that the innate immune system is a potential contributor to short- and long-term graft injuries. We seek to provide an overview of the current literature on innate immunity in transplantation, discussing both innate naïve and memory immune responses, mechanisms by which innate cells recognize allogeneic signals, specific subsets of innate cells implicated in these responses, and soluble mediators that may aid in the graft inflammation. Recent Findings The mechanisms by which innate cells recognize allogeneic tissue are being uncovered, and prior exposure to allogeneic cells may impact the strength of that response, thereby giving the innate cells “memory” of the previously encountered alloantigens. The implicated and discussed ligands & receptors for the innate immune recognition include ischemia-reperfusion injury products & the DAMP receptors, class I MHC & PIRA, CD47 & SIRPα. Additionally, the roles of macrophages, NK cells, γδ T cells, and complement proteins are examined. Summary It is likely that innate immune cells and pathways contribute to significantly altering the longevity of transplanted allografts, therefore warrant future investigations. Innate immune cells and their respective molecular targets might represent new points of intervention. | ||
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10.1007/s40472-023-00422-4 doi (DE-627)SPR054173175 (SPR)s40472-023-00422-4-e DE-627 ger DE-627 rakwb eng Ladowski, Joseph M. verfasserin aut Innate Immune Responses in Transplant Immunity 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s), under exclusive licence to Springer Nature Switzerland AG 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. Purpose of Review Despite a significant decrease in the rate of acute rejection, long-term solid organ allotransplant success is limited by chronic rejection. Transplant research has historically focused on adaptive immune responses. However, there is a growing appreciation that the innate immune system is a potential contributor to short- and long-term graft injuries. We seek to provide an overview of the current literature on innate immunity in transplantation, discussing both innate naïve and memory immune responses, mechanisms by which innate cells recognize allogeneic signals, specific subsets of innate cells implicated in these responses, and soluble mediators that may aid in the graft inflammation. Recent Findings The mechanisms by which innate cells recognize allogeneic tissue are being uncovered, and prior exposure to allogeneic cells may impact the strength of that response, thereby giving the innate cells “memory” of the previously encountered alloantigens. The implicated and discussed ligands & receptors for the innate immune recognition include ischemia-reperfusion injury products & the DAMP receptors, class I MHC & PIRA, CD47 & SIRPα. Additionally, the roles of macrophages, NK cells, γδ T cells, and complement proteins are examined. Summary It is likely that innate immune cells and pathways contribute to significantly altering the longevity of transplanted allografts, therefore warrant future investigations. Innate immune cells and their respective molecular targets might represent new points of intervention. Innate immunity (dpeaa)DE-He213 Trained immunity (dpeaa)DE-He213 Innate transplant immune cells (dpeaa)DE-He213 Luo, Xunrong aut Enthalten in Current transplantation reports Cham : Springer Internat. Publ., 2014 10(2023), 4 vom: 27. Nov., Seite 237-244 (DE-627)78037844X (DE-600)2760306-4 2196-3029 nnns volume:10 year:2023 number:4 day:27 month:11 pages:237-244 https://dx.doi.org/10.1007/s40472-023-00422-4 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 10 2023 4 27 11 237-244 |
| spelling |
10.1007/s40472-023-00422-4 doi (DE-627)SPR054173175 (SPR)s40472-023-00422-4-e DE-627 ger DE-627 rakwb eng Ladowski, Joseph M. verfasserin aut Innate Immune Responses in Transplant Immunity 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s), under exclusive licence to Springer Nature Switzerland AG 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. Purpose of Review Despite a significant decrease in the rate of acute rejection, long-term solid organ allotransplant success is limited by chronic rejection. Transplant research has historically focused on adaptive immune responses. However, there is a growing appreciation that the innate immune system is a potential contributor to short- and long-term graft injuries. We seek to provide an overview of the current literature on innate immunity in transplantation, discussing both innate naïve and memory immune responses, mechanisms by which innate cells recognize allogeneic signals, specific subsets of innate cells implicated in these responses, and soluble mediators that may aid in the graft inflammation. Recent Findings The mechanisms by which innate cells recognize allogeneic tissue are being uncovered, and prior exposure to allogeneic cells may impact the strength of that response, thereby giving the innate cells “memory” of the previously encountered alloantigens. The implicated and discussed ligands & receptors for the innate immune recognition include ischemia-reperfusion injury products & the DAMP receptors, class I MHC & PIRA, CD47 & SIRPα. Additionally, the roles of macrophages, NK cells, γδ T cells, and complement proteins are examined. Summary It is likely that innate immune cells and pathways contribute to significantly altering the longevity of transplanted allografts, therefore warrant future investigations. Innate immune cells and their respective molecular targets might represent new points of intervention. Innate immunity (dpeaa)DE-He213 Trained immunity (dpeaa)DE-He213 Innate transplant immune cells (dpeaa)DE-He213 Luo, Xunrong aut Enthalten in Current transplantation reports Cham : Springer Internat. Publ., 2014 10(2023), 4 vom: 27. Nov., Seite 237-244 (DE-627)78037844X (DE-600)2760306-4 2196-3029 nnns volume:10 year:2023 number:4 day:27 month:11 pages:237-244 https://dx.doi.org/10.1007/s40472-023-00422-4 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 10 2023 4 27 11 237-244 |
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10.1007/s40472-023-00422-4 doi (DE-627)SPR054173175 (SPR)s40472-023-00422-4-e DE-627 ger DE-627 rakwb eng Ladowski, Joseph M. verfasserin aut Innate Immune Responses in Transplant Immunity 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s), under exclusive licence to Springer Nature Switzerland AG 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. Purpose of Review Despite a significant decrease in the rate of acute rejection, long-term solid organ allotransplant success is limited by chronic rejection. Transplant research has historically focused on adaptive immune responses. However, there is a growing appreciation that the innate immune system is a potential contributor to short- and long-term graft injuries. We seek to provide an overview of the current literature on innate immunity in transplantation, discussing both innate naïve and memory immune responses, mechanisms by which innate cells recognize allogeneic signals, specific subsets of innate cells implicated in these responses, and soluble mediators that may aid in the graft inflammation. Recent Findings The mechanisms by which innate cells recognize allogeneic tissue are being uncovered, and prior exposure to allogeneic cells may impact the strength of that response, thereby giving the innate cells “memory” of the previously encountered alloantigens. The implicated and discussed ligands & receptors for the innate immune recognition include ischemia-reperfusion injury products & the DAMP receptors, class I MHC & PIRA, CD47 & SIRPα. Additionally, the roles of macrophages, NK cells, γδ T cells, and complement proteins are examined. Summary It is likely that innate immune cells and pathways contribute to significantly altering the longevity of transplanted allografts, therefore warrant future investigations. Innate immune cells and their respective molecular targets might represent new points of intervention. Innate immunity (dpeaa)DE-He213 Trained immunity (dpeaa)DE-He213 Innate transplant immune cells (dpeaa)DE-He213 Luo, Xunrong aut Enthalten in Current transplantation reports Cham : Springer Internat. Publ., 2014 10(2023), 4 vom: 27. Nov., Seite 237-244 (DE-627)78037844X (DE-600)2760306-4 2196-3029 nnns volume:10 year:2023 number:4 day:27 month:11 pages:237-244 https://dx.doi.org/10.1007/s40472-023-00422-4 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 10 2023 4 27 11 237-244 |
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10.1007/s40472-023-00422-4 doi (DE-627)SPR054173175 (SPR)s40472-023-00422-4-e DE-627 ger DE-627 rakwb eng Ladowski, Joseph M. verfasserin aut Innate Immune Responses in Transplant Immunity 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s), under exclusive licence to Springer Nature Switzerland AG 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. Purpose of Review Despite a significant decrease in the rate of acute rejection, long-term solid organ allotransplant success is limited by chronic rejection. Transplant research has historically focused on adaptive immune responses. However, there is a growing appreciation that the innate immune system is a potential contributor to short- and long-term graft injuries. We seek to provide an overview of the current literature on innate immunity in transplantation, discussing both innate naïve and memory immune responses, mechanisms by which innate cells recognize allogeneic signals, specific subsets of innate cells implicated in these responses, and soluble mediators that may aid in the graft inflammation. Recent Findings The mechanisms by which innate cells recognize allogeneic tissue are being uncovered, and prior exposure to allogeneic cells may impact the strength of that response, thereby giving the innate cells “memory” of the previously encountered alloantigens. The implicated and discussed ligands & receptors for the innate immune recognition include ischemia-reperfusion injury products & the DAMP receptors, class I MHC & PIRA, CD47 & SIRPα. Additionally, the roles of macrophages, NK cells, γδ T cells, and complement proteins are examined. Summary It is likely that innate immune cells and pathways contribute to significantly altering the longevity of transplanted allografts, therefore warrant future investigations. Innate immune cells and their respective molecular targets might represent new points of intervention. Innate immunity (dpeaa)DE-He213 Trained immunity (dpeaa)DE-He213 Innate transplant immune cells (dpeaa)DE-He213 Luo, Xunrong aut Enthalten in Current transplantation reports Cham : Springer Internat. Publ., 2014 10(2023), 4 vom: 27. Nov., Seite 237-244 (DE-627)78037844X (DE-600)2760306-4 2196-3029 nnns volume:10 year:2023 number:4 day:27 month:11 pages:237-244 https://dx.doi.org/10.1007/s40472-023-00422-4 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 10 2023 4 27 11 237-244 |
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10.1007/s40472-023-00422-4 doi (DE-627)SPR054173175 (SPR)s40472-023-00422-4-e DE-627 ger DE-627 rakwb eng Ladowski, Joseph M. verfasserin aut Innate Immune Responses in Transplant Immunity 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s), under exclusive licence to Springer Nature Switzerland AG 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. Purpose of Review Despite a significant decrease in the rate of acute rejection, long-term solid organ allotransplant success is limited by chronic rejection. Transplant research has historically focused on adaptive immune responses. However, there is a growing appreciation that the innate immune system is a potential contributor to short- and long-term graft injuries. We seek to provide an overview of the current literature on innate immunity in transplantation, discussing both innate naïve and memory immune responses, mechanisms by which innate cells recognize allogeneic signals, specific subsets of innate cells implicated in these responses, and soluble mediators that may aid in the graft inflammation. Recent Findings The mechanisms by which innate cells recognize allogeneic tissue are being uncovered, and prior exposure to allogeneic cells may impact the strength of that response, thereby giving the innate cells “memory” of the previously encountered alloantigens. The implicated and discussed ligands & receptors for the innate immune recognition include ischemia-reperfusion injury products & the DAMP receptors, class I MHC & PIRA, CD47 & SIRPα. Additionally, the roles of macrophages, NK cells, γδ T cells, and complement proteins are examined. Summary It is likely that innate immune cells and pathways contribute to significantly altering the longevity of transplanted allografts, therefore warrant future investigations. Innate immune cells and their respective molecular targets might represent new points of intervention. Innate immunity (dpeaa)DE-He213 Trained immunity (dpeaa)DE-He213 Innate transplant immune cells (dpeaa)DE-He213 Luo, Xunrong aut Enthalten in Current transplantation reports Cham : Springer Internat. Publ., 2014 10(2023), 4 vom: 27. Nov., Seite 237-244 (DE-627)78037844X (DE-600)2760306-4 2196-3029 nnns volume:10 year:2023 number:4 day:27 month:11 pages:237-244 https://dx.doi.org/10.1007/s40472-023-00422-4 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 10 2023 4 27 11 237-244 |
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Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Purpose of Review Despite a significant decrease in the rate of acute rejection, long-term solid organ allotransplant success is limited by chronic rejection. Transplant research has historically focused on adaptive immune responses. However, there is a growing appreciation that the innate immune system is a potential contributor to short- and long-term graft injuries. We seek to provide an overview of the current literature on innate immunity in transplantation, discussing both innate naïve and memory immune responses, mechanisms by which innate cells recognize allogeneic signals, specific subsets of innate cells implicated in these responses, and soluble mediators that may aid in the graft inflammation. Recent Findings The mechanisms by which innate cells recognize allogeneic tissue are being uncovered, and prior exposure to allogeneic cells may impact the strength of that response, thereby giving the innate cells “memory” of the previously encountered alloantigens. The implicated and discussed ligands & receptors for the innate immune recognition include ischemia-reperfusion injury products & the DAMP receptors, class I MHC & PIRA, CD47 & SIRPα. Additionally, the roles of macrophages, NK cells, γδ T cells, and complement proteins are examined. Summary It is likely that innate immune cells and pathways contribute to significantly altering the longevity of transplanted allografts, therefore warrant future investigations. 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Ladowski, Joseph M. |
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innate immune responses in transplant immunity |
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Innate Immune Responses in Transplant Immunity |
| abstract |
Purpose of Review Despite a significant decrease in the rate of acute rejection, long-term solid organ allotransplant success is limited by chronic rejection. Transplant research has historically focused on adaptive immune responses. However, there is a growing appreciation that the innate immune system is a potential contributor to short- and long-term graft injuries. We seek to provide an overview of the current literature on innate immunity in transplantation, discussing both innate naïve and memory immune responses, mechanisms by which innate cells recognize allogeneic signals, specific subsets of innate cells implicated in these responses, and soluble mediators that may aid in the graft inflammation. Recent Findings The mechanisms by which innate cells recognize allogeneic tissue are being uncovered, and prior exposure to allogeneic cells may impact the strength of that response, thereby giving the innate cells “memory” of the previously encountered alloantigens. The implicated and discussed ligands & receptors for the innate immune recognition include ischemia-reperfusion injury products & the DAMP receptors, class I MHC & PIRA, CD47 & SIRPα. Additionally, the roles of macrophages, NK cells, γδ T cells, and complement proteins are examined. Summary It is likely that innate immune cells and pathways contribute to significantly altering the longevity of transplanted allografts, therefore warrant future investigations. Innate immune cells and their respective molecular targets might represent new points of intervention. © The Author(s), under exclusive licence to Springer Nature Switzerland AG 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. |
| abstractGer |
Purpose of Review Despite a significant decrease in the rate of acute rejection, long-term solid organ allotransplant success is limited by chronic rejection. Transplant research has historically focused on adaptive immune responses. However, there is a growing appreciation that the innate immune system is a potential contributor to short- and long-term graft injuries. We seek to provide an overview of the current literature on innate immunity in transplantation, discussing both innate naïve and memory immune responses, mechanisms by which innate cells recognize allogeneic signals, specific subsets of innate cells implicated in these responses, and soluble mediators that may aid in the graft inflammation. Recent Findings The mechanisms by which innate cells recognize allogeneic tissue are being uncovered, and prior exposure to allogeneic cells may impact the strength of that response, thereby giving the innate cells “memory” of the previously encountered alloantigens. The implicated and discussed ligands & receptors for the innate immune recognition include ischemia-reperfusion injury products & the DAMP receptors, class I MHC & PIRA, CD47 & SIRPα. Additionally, the roles of macrophages, NK cells, γδ T cells, and complement proteins are examined. Summary It is likely that innate immune cells and pathways contribute to significantly altering the longevity of transplanted allografts, therefore warrant future investigations. Innate immune cells and their respective molecular targets might represent new points of intervention. © The Author(s), under exclusive licence to Springer Nature Switzerland AG 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. |
| abstract_unstemmed |
Purpose of Review Despite a significant decrease in the rate of acute rejection, long-term solid organ allotransplant success is limited by chronic rejection. Transplant research has historically focused on adaptive immune responses. However, there is a growing appreciation that the innate immune system is a potential contributor to short- and long-term graft injuries. We seek to provide an overview of the current literature on innate immunity in transplantation, discussing both innate naïve and memory immune responses, mechanisms by which innate cells recognize allogeneic signals, specific subsets of innate cells implicated in these responses, and soluble mediators that may aid in the graft inflammation. Recent Findings The mechanisms by which innate cells recognize allogeneic tissue are being uncovered, and prior exposure to allogeneic cells may impact the strength of that response, thereby giving the innate cells “memory” of the previously encountered alloantigens. The implicated and discussed ligands & receptors for the innate immune recognition include ischemia-reperfusion injury products & the DAMP receptors, class I MHC & PIRA, CD47 & SIRPα. Additionally, the roles of macrophages, NK cells, γδ T cells, and complement proteins are examined. Summary It is likely that innate immune cells and pathways contribute to significantly altering the longevity of transplanted allografts, therefore warrant future investigations. Innate immune cells and their respective molecular targets might represent new points of intervention. © The Author(s), under exclusive licence to Springer Nature Switzerland AG 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. |
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Innate Immune Responses in Transplant Immunity |
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https://dx.doi.org/10.1007/s40472-023-00422-4 |
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Luo, Xunrong |
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10.1007/s40472-023-00422-4 |
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2024-07-04T00:17:55.365Z |
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| score |
7.398506 |