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B in CD8+ T Cells Exposed To Peripheral Self-Antigens1
*
Centre d’Immunologie de Marseille-Luminy, Institut National de la Santé et de la Recherche Médicale/Centre National de la Recherche Scientifique/Université de la Méditerranée, Marseille, France; and
Department of Medicine, Program of Immunobiology, University of Vermont, Burlington, VT 05405
The transcriptional events that control T cell tolerance to
peripheral self Ags are still unknown. In this study, we analyzed the
regulation of AP-1- and NF-
B-mediated transcription during in vivo
induction of tolerance to a self Ag expressed exclusively on
hepatocytes. Naive CD8+Désiré
(Des)+ T cells isolated from the Des TCR-transgenic mice
that are specific for the H-2Kb class I Ag were transferred
into Alb-Kb-transgenic mice that express the
H-2Kb Ag on hepatocytes only. Tolerance develops in these
mice. We found that the self-reactive
CD8+Des+ T cells were transiently activated,
then became unresponsive and were further deleted. In contrast to
CD8+Des+ T cells activated in vivo with APCs,
which express high AP-1 and high NF-B transcriptional activity, the
unresponsive CD8+Des+ T cells expressed no AP-1
and only weak NF-B transcriptional activity. The differences in
NF-B transcriptional activity correlated with the generation of
distinct NF-B complexes. Indeed, in vivo primed T cells
predominantly express p50/p50 and p65/p50 dimers, whereas these
p50-containing complexes are barely detectable in tolerant T cells that
express p65- and c-Rel-containing complexes. These observations suggest
that fine regulation of NF-B complex formation may determine T cell
fate.
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