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Publication : Homeostatic regulation of CD8+ T cells after antigen challenge in the absence of Fas (CD95).

First Author  Zimmermann C Year  1996
Journal  Eur J Immunol Volume  26
Issue  12 Pages  2903-10
PubMed ID  8977284 Mgi Jnum  J:37076
Mgi Id  MGI:84480 Doi  10.1002/eji.1830261215
Citation  Zimmermann C, et al. (1996) Homeostatic regulation of CD8+ T cells after antigen challenge in the absence of Fas (CD95). Eur J Immunol 26(12):2903-10
abstractText  The role of Fas in the homeostatic regulation of CD8(+) T cells after antigen challenge was analyzed in the murine model of lymphocytic choriomeningitis virus (LCMV) infection. Mice homozygous for the lpr mutation and carrying T cell receptor (TCR) alpha beta transgenes specific for the LCMV glycoprotein peptide aa 33-41 in the context of H-2D(b) were used. Five main results emerged: first, development of lymphadenopathy and of CD4(-)CD8(-) double-negative B220(+) T cells in lpr mice was not inhibited by the alpha beta TCR transgenes; second, tolerance induction and peripheral deletion of CD8(+) T cells induced by LCMV glycoprotein peptide injection was independent of Fas expression; third, clonal down- regulation of Fas-deficient TCR-transgenic CD8(+) T cells after acute LCM virus infection was identical to the decline of transgenic T cells expressing Fas; fourth, in vivo activated CD8(+) effector T cells from TCR transgenic and TCR-lpr/lpr mice were equally susceptible to activation-induced cell death in vitro; and fifth, transgenic effector Tcells from lpr/lpr mice were cleared in the declining phase of the immune response in vivo without giving rise to CD4(-)CD8(-) double-negative T celIs. Taken together, these data suggest that the homeostatic regulation of CD8(+) T cells after antigen challenge in vivo is regulated by mechanisms that do not require Fas.
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