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In vivo elimination of CD4+ T cells prevents fetal allograft rejection in mice after LCMV virus infection
162
P 235
IN VlVO ELIMINATIONOF CD4+ T CELLS PREVENTSFETAL ALLOGRAFTREJECTION IN MICE AFTER LCMVVIRUS INFECTION Lothar S t i t z l and Rolf Zinkernagel2 I n s t i t u t fur Virologie, Justus-Liebig-Universit~t Giessen, FRG 1 and I n s t i t u t fur Pathologie, Universit~t ZUrich, Switzerland 2 After infection of pregnant mice with the non-cytolytic RNA virus of lymphocytic choriomeningitis (LCMV) two different patterns of reaction can be observed. The consequence of intraveneous infection during the early stage of pregnancy (day 0 through 4 post conceptionem (p.c.)) is the intrauterine death of the offspring. Histologically this event is represented by necrotic processes in the placenta. In mice infected at later stages of pregnancy (day 8 through 16 p.c.) no fetal death is observed; however, some of the newborn mice are virus carriers and develop tolerance to LCMV. In mice infected during the early stage of pregnancy fetal death can be prevented by treatment with monoclonal antibodies directed against CD4+ T cells. In contrast anti-CD8 moabs do not prevent rejection of fetuses; however, CD8+ T cells represent the most important a n t i v i r a l protective and immunopathological T cell subpopulation after LCMV infection in the blood and the spleen. LCMVinfection of pregnant mice lends i t s e l f exquisitely as a model of immune-mediated rejection of mouse fetuses and likewise suggests the a c t i v i t y of different T cells subsets in different organs. keywords: CD4+T cells, fetal allograft rejection
P 235
IN VlVO ELIMINATIONOF CD4+ T CELLS PREVENTSFETAL ALLOGRAFTREJECTION IN MICE AFTER LCMVVIRUS INFECTION Lothar S t i t z l and Rolf Zinkernagel2 I n s t i t u t fur Virologie, Justus-Liebig-Universit~t Giessen, FRG 1 and I n s t i t u t fur Pathologie, Universit~t ZUrich, Switzerland 2 After infection of pregnant mice with the non-cytolytic RNA virus of lymphocytic choriomeningitis (LCMV) two different patterns of reaction can be observed. The consequence of intraveneous infection during the early stage of pregnancy (day 0 through 4 post conceptionem (p.c.)) is the intrauterine death of the offspring. Histologically this event is represented by necrotic processes in the placenta. In mice infected at later stages of pregnancy (day 8 through 16 p.c.) no fetal death is observed; however, some of the newborn mice are virus carriers and develop tolerance to LCMV. In mice infected during the early stage of pregnancy fetal death can be prevented by treatment with monoclonal antibodies directed against CD4+ T cells. In contrast anti-CD8 moabs do not prevent rejection of fetuses; however, CD8+ T cells represent the most important a n t i v i r a l protective and immunopathological T cell subpopulation after LCMV infection in the blood and the spleen. LCMVinfection of pregnant mice lends i t s e l f exquisitely as a model of immune-mediated rejection of mouse fetuses and likewise suggests the a c t i v i t y of different T cells subsets in different organs. keywords: CD4+T cells, fetal allograft rejection