Abstract
bcl-x, a homologous gene of bcl-2, has an anti-apoptotic function and appears to play a critical role in the development of lymphoid systems. To investigate the effect of overexpressed Bcl-xL on the development of T lymphocytes, we established two lines of transgenic mice by using Eμ-chicken bcl-xL (cbcl-xL) transgene, where the cBcl-xL protein was expressed mainly in lymphoid cells. Although thymocytes and splenocytes from cbcl-xL transgenic mice are resistant to apoptosis in vitro, clonal deletion of thymocytes, recognizing endogenous self-superantigens in the thymus, still normally proceeded and no self-reactive T cells were found in the spleen of the transgenic mice. To dissect clonal deletion, we utilized two in vitro models, thymocytes/antigen presenting cells co-culture system and fetal thymus organ culture system. In both, bacterial superantigen staphylococcus aureus enterotoxin B (SEB) induces apoptosis of T cells with Vβ8+ T cell receptor (TCR) reacting to SEB, which mimics clonal deletion of self-reactive thymocytes in vivo. SEB-induced depletion of Vβ8+ T cells from thymocytes when taken from the transgenic mice was effectively inhibited. The data might raise the possibility that cell death process involved in clonal deletion in the thymus is a form of apoptosis inhibited by Bcl-xL.
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Takahashi, T., Honda, H., Hirai, H. et al. Overexpressed Bcl-xL prevents bacterial superantigen-induced apoptosis of thymocytes in vitro. Cell Death Differ 4, 159–165 (1997). https://doi.org/10.1038/sj.cdd.4400214
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DOI: https://doi.org/10.1038/sj.cdd.4400214