| First Author | Nakajima H | Year | 1999 |
| Journal | J Immunol | Volume | 162 |
| Issue | 2 | Pages | 782-90 |
| PubMed ID | 9916699 | Mgi Jnum | J:52019 |
| Mgi Id | MGI:1327709 | Doi | 10.4049/jimmunol.162.2.782 |
| Citation | Nakajima H, et al. (1999) Role of Bcl-2 in alpha beta T cell development in mice deficient in the common cytokine receptor gamma-chain: the requirement for Bcl-2 differs depending on the TCR/MHC affinity. J Immunol 162(2):782-90 |
| abstractText | Mice lacking the common cytokine receptor gamma-chain (gamma 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 alpha beta T cell development but not gamma delta 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 gamma 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 gamma c wild-type mice. These results suggest that the importance of gamma 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 gamma 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 gamma c-dependent Bcl-2 expression influences T cell development in a TCR/MHC-dependent manner. |
