Constitutive expression of Bcl-xL or Bcl-2 prevents peptide antigen-induced T cell deletion but does not influence T cell homeostasis after a viral infection
✍ Scribed by Franziska Petschner; Christine Zimmermann; Andreas Strasser; Didier Grillot; Gabriel Nunez; Hanspeter Pircher
- Publisher
- John Wiley and Sons
- Year
- 1998
- Tongue
- English
- Weight
- 270 KB
- Volume
- 28
- Category
- Article
- ISSN
- 0014-2980
No coin nor oath required. For personal study only.
✦ Synopsis
We examined the CD8 + T cell response to lymphocytic choriomeningitis virus (LCMV) in mice doubly transgenic for an LCMV-specific TCR and for either bcl-x L or bcl-2. Clonal downsizing of the anti-viral CD8 + T cell response and the generation of T cell memory was not influenced by constitutive expression of these anti-apoptotic proteins in T cells. Expression of Bcl-x L or Bcl-2 did, however, prevent LCMV peptide-induced peripheral deletion of mature CD8 + T cells in vivo and apoptosis of activated LCMV-specific effector T cells in vitro. The CD8 + T cells "rescued" by Bcl-x L or Bcl-2 from peptide antigen-induced cell death were anergic and this could not be reversed by addition of IL-2 in vitro or by adoptive transfer into antigen-free recipient mice followed by LCMV infection in vivo. Taken together, we show here that 1) Bcl-x L or Bcl-2 are functionally equivalent in their ability to modulate CD8 + T cell survival in vivo, 2) distinct apoptosis signaling pathways exist in CD8 + T cells, one that can be inhibited by Bcl-2 or Bcl-x L and one that cannot be blocked, and 3) apoptosis of CD8 + effector T cells during the declining phase of an immune response is not prevented by constitutive expression of the anti-apoptotic proteins Bcl-x L and Bcl-2.