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ß T Cell Development in Mice Deficient in the Common Cytokine Receptor 
-Chain: The Requirement for Bcl-2 Differs Depending on the TCR/MHC Affinity
Laboratory of Molecular Immunology, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892
Mice lacking the common cytokine receptor 
-chain
(c) exhibit severely compromised T cell development,
with diminished Bcl-2 expression in mature (CD4+ or
CD8+) thymocytes and peripheral T cells. Enforced
expression of Bcl-2 in these mice partially rescued 
ß T cell
development but not 
T cell development. Transgenic expression of
the OVA-specific DO11.10 (DO10) TCR also could modestly increase
thymocyte numbers, and T cells expressing the transgenic TCR
(KJ1-26+ T cells) were found in the periphery.
Interestingly, the presence of KJ1-26+ T cells was
dependent on the MHC background and was seen in the moderate affinity
H-2d/d background but not in the higher affinity
H-2d/b background in c-deficient mice. In
contrast, KJ1-26+ T cells exist in the periphery in both
the H-2d/d and H-2d/b backgrounds in DO10
transgenic c wild-type mice. These results suggest that
the importance of c-dependent signals for T cell
development differs depending on the affinity of TCR for MHC. Moreover,
enforced expression of Bcl-2 had a much greater effect on the
development of c-deficient T cells expressing the DO10
TCR in the high affinity H-2d/b background than in the
H-2d/d background, suggesting that
c-dependent Bcl-2 expression influences T cell
development in a TCR/MHC-dependent manner.
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