Apoptosis of CD4+ and CD8+ T cells during experimental infection with Mycobacterium avium is controlled by Fas/FasL and Bcl-2-sensitive pathways, respectively

Both CD4 and CD8 T cells from mice infected with Mycobacterium avium suffered a high rate of apoptosis, beginning with the onset of the immune response and culminating in the loss of T cells from the tissues and loss of IFN-γ production. Fas expression increased over the course of infection on both T cell populations, as did their susceptibility to the induction of apoptosis in vitro by anti-Fas mAb. Nevertheless, although the rate of apoptosis among CD4 T cells from infected mice was reduced to normal levels in lpr mice with a defective Fas, CD8 T cells were unaffected, implying that Fas/FasL interaction was not important in these cells in vivo. Conversely, over-expression of B-cell lymphoma-2 (Bcl-2), which is known to protect T cells from apoptosis signalled through the TNF receptor or due to the withdrawal of cytokines, totally protected CD8 T cells from infected mice but had no effect on CD4. It is of interest that these two contrasting pathways of T-cell apoptosis operate at the same time during a single infection