Constitutive expression of Bcl-x(L) or Bcl-2 prevents peptide antigen-induced T cell deletion but does not influence T cell homeostasis after a viral infection
- Author(s)
- Petschner, F; Zimmermann, C; Strasser, A; Grillot, D; Nunez, G; Pircher, H;
- Details
- Publication Year 1998-02,Volume 28,Issue #2,Page 560-569
- Journal Title
- EUROPEAN JOURNAL OF IMMUNOLOGY
- Publication Type
- Journal Article
- Abstract
- 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 I) 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.
- Publisher
- WILEY-V C H VERLAG GMBH
- Keywords
- RECEPTOR TRANSGENIC MICE; INHIBITS MULTIPLE FORMS; TUMOR-NECROSIS-FACTOR; LYMPHOCYTE APOPTOSIS; TOLERANCE INDUCTION; CD28 COSTIMULATION; NEGATIVE SELECTION; DEATH; SURVIVAL; ABSENCE
- Publisher's Version
- https://doi.org/10.1002/(SICI)1521-4141(199802)28:02<560::AID-IMMU560>3.0.CO;2-Q
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- Refer to copyright notice on published article.
Creation Date: 1998-02-01 12:00:00