Immunology at the Maternal-Fetal Interface: Lessons for T Cell Tolerance and Suppression
Abstract Mammalian reproduction poses an immunological paradox because fetal alloantigens encoded by genes inherited from the father should provoke responses by maternal T cells leading to fetal loss. Current understanding of T cell immunobiology and the critical role of inflammatory processes durin...
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E-Artikel |
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| Erschienen: |
2000 |
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25 |
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Annual Reviews Electronic Back Volume Collection 1932-2005ff |
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in: Annual review of immunology - Palo Alto, Calif. : Annual Reviews Inc., 1983, 18(2000), Seite 367-391 |
| Übergeordnetes Werk: |
volume:18 ; year:2000 ; pages:367-391 ; extent:25 |
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| 520 | |a Abstract Mammalian reproduction poses an immunological paradox because fetal alloantigens encoded by genes inherited from the father should provoke responses by maternal T cells leading to fetal loss. Current understanding of T cell immunobiology and the critical role of inflammatory processes during pregnancy is reviewed and discussed. Lessons derived from studies on the regulation of T cell responsiveness during mammalian gestation are considered in the wider context of T cell tolerance toward some microbial infections and tumors, avoidance of autoimmunity, and tissue allograft rejection. | ||
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(DE-627)NLEJ16410982X DE-627 ger DE-627 rakwb Immunology at the Maternal-Fetal Interface: Lessons for T Cell Tolerance and Suppression 2000 25 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract Mammalian reproduction poses an immunological paradox because fetal alloantigens encoded by genes inherited from the father should provoke responses by maternal T cells leading to fetal loss. Current understanding of T cell immunobiology and the critical role of inflammatory processes during pregnancy is reviewed and discussed. Lessons derived from studies on the regulation of T cell responsiveness during mammalian gestation are considered in the wider context of T cell tolerance toward some microbial infections and tumors, avoidance of autoimmunity, and tissue allograft rejection. Annual Reviews Electronic Back Volume Collection 1932-2005ff Mellor, A. L. oth Munn, D. H. oth in Annual review of immunology Palo Alto, Calif. : Annual Reviews Inc., 1983 18(2000), Seite 367-391 Online-Ressource (DE-627)NLEJ164018891 (DE-600)1470451-1 1545-3278 nnns volume:18 year:2000 pages:367-391 extent:25 http://dx.doi.org/10.1146/annurev.immunol.18.1.367 text/html Deutschlandweit zugänglich GBV_USEFLAG_U ZDB-1-ANR GBV_NL_ARTICLE AR 18 2000 367-391 25 |
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(DE-627)NLEJ16410982X DE-627 ger DE-627 rakwb Immunology at the Maternal-Fetal Interface: Lessons for T Cell Tolerance and Suppression 2000 25 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract Mammalian reproduction poses an immunological paradox because fetal alloantigens encoded by genes inherited from the father should provoke responses by maternal T cells leading to fetal loss. Current understanding of T cell immunobiology and the critical role of inflammatory processes during pregnancy is reviewed and discussed. Lessons derived from studies on the regulation of T cell responsiveness during mammalian gestation are considered in the wider context of T cell tolerance toward some microbial infections and tumors, avoidance of autoimmunity, and tissue allograft rejection. Annual Reviews Electronic Back Volume Collection 1932-2005ff Mellor, A. L. oth Munn, D. H. oth in Annual review of immunology Palo Alto, Calif. : Annual Reviews Inc., 1983 18(2000), Seite 367-391 Online-Ressource (DE-627)NLEJ164018891 (DE-600)1470451-1 1545-3278 nnns volume:18 year:2000 pages:367-391 extent:25 http://dx.doi.org/10.1146/annurev.immunol.18.1.367 text/html Deutschlandweit zugänglich GBV_USEFLAG_U ZDB-1-ANR GBV_NL_ARTICLE AR 18 2000 367-391 25 |
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(DE-627)NLEJ16410982X DE-627 ger DE-627 rakwb Immunology at the Maternal-Fetal Interface: Lessons for T Cell Tolerance and Suppression 2000 25 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract Mammalian reproduction poses an immunological paradox because fetal alloantigens encoded by genes inherited from the father should provoke responses by maternal T cells leading to fetal loss. Current understanding of T cell immunobiology and the critical role of inflammatory processes during pregnancy is reviewed and discussed. Lessons derived from studies on the regulation of T cell responsiveness during mammalian gestation are considered in the wider context of T cell tolerance toward some microbial infections and tumors, avoidance of autoimmunity, and tissue allograft rejection. Annual Reviews Electronic Back Volume Collection 1932-2005ff Mellor, A. L. oth Munn, D. H. oth in Annual review of immunology Palo Alto, Calif. : Annual Reviews Inc., 1983 18(2000), Seite 367-391 Online-Ressource (DE-627)NLEJ164018891 (DE-600)1470451-1 1545-3278 nnns volume:18 year:2000 pages:367-391 extent:25 http://dx.doi.org/10.1146/annurev.immunol.18.1.367 text/html Deutschlandweit zugänglich GBV_USEFLAG_U ZDB-1-ANR GBV_NL_ARTICLE AR 18 2000 367-391 25 |
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(DE-627)NLEJ16410982X DE-627 ger DE-627 rakwb Immunology at the Maternal-Fetal Interface: Lessons for T Cell Tolerance and Suppression 2000 25 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract Mammalian reproduction poses an immunological paradox because fetal alloantigens encoded by genes inherited from the father should provoke responses by maternal T cells leading to fetal loss. Current understanding of T cell immunobiology and the critical role of inflammatory processes during pregnancy is reviewed and discussed. Lessons derived from studies on the regulation of T cell responsiveness during mammalian gestation are considered in the wider context of T cell tolerance toward some microbial infections and tumors, avoidance of autoimmunity, and tissue allograft rejection. Annual Reviews Electronic Back Volume Collection 1932-2005ff Mellor, A. L. oth Munn, D. H. oth in Annual review of immunology Palo Alto, Calif. : Annual Reviews Inc., 1983 18(2000), Seite 367-391 Online-Ressource (DE-627)NLEJ164018891 (DE-600)1470451-1 1545-3278 nnns volume:18 year:2000 pages:367-391 extent:25 http://dx.doi.org/10.1146/annurev.immunol.18.1.367 text/html Deutschlandweit zugänglich GBV_USEFLAG_U ZDB-1-ANR GBV_NL_ARTICLE AR 18 2000 367-391 25 |
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Abstract Mammalian reproduction poses an immunological paradox because fetal alloantigens encoded by genes inherited from the father should provoke responses by maternal T cells leading to fetal loss. Current understanding of T cell immunobiology and the critical role of inflammatory processes during pregnancy is reviewed and discussed. Lessons derived from studies on the regulation of T cell responsiveness during mammalian gestation are considered in the wider context of T cell tolerance toward some microbial infections and tumors, avoidance of autoimmunity, and tissue allograft rejection. |
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Abstract Mammalian reproduction poses an immunological paradox because fetal alloantigens encoded by genes inherited from the father should provoke responses by maternal T cells leading to fetal loss. Current understanding of T cell immunobiology and the critical role of inflammatory processes during pregnancy is reviewed and discussed. Lessons derived from studies on the regulation of T cell responsiveness during mammalian gestation are considered in the wider context of T cell tolerance toward some microbial infections and tumors, avoidance of autoimmunity, and tissue allograft rejection. |
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Abstract Mammalian reproduction poses an immunological paradox because fetal alloantigens encoded by genes inherited from the father should provoke responses by maternal T cells leading to fetal loss. Current understanding of T cell immunobiology and the critical role of inflammatory processes during pregnancy is reviewed and discussed. Lessons derived from studies on the regulation of T cell responsiveness during mammalian gestation are considered in the wider context of T cell tolerance toward some microbial infections and tumors, avoidance of autoimmunity, and tissue allograft rejection. |
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