English
 
Help Privacy Policy Disclaimer
  Advanced SearchBrowse

Item

ITEM ACTIONSEXPORT

Released

Journal Article

Antigen-induced cell death of T effector cells in vitro proceeds via the Fas pathway, requires endogenous interferon-γ and is independent of perforin and granzymes

MPS-Authors
/persons/resource/persons191326

Sobek,  Vera
Emeritus Group: Cellular Immunology, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

/persons/resource/persons190975

Balkow,  Sandra
Metchnikoff Laboratory, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

/persons/resource/persons191321

Simon,  Markus M.
Metchnikoff Laboratory, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

External Resource
No external resources are shared
Fulltext (public)
There are no public fulltexts stored in PuRe
Supplementary Material (public)
There is no public supplementary material available
Citation

Sobek, V., Balkow, S., Koerner, H., & Simon, M. M. (2002). Antigen-induced cell death of T effector cells in vitro proceeds via the Fas pathway, requires endogenous interferon-γ and is independent of perforin and granzymes. European Journal of Immunology, 32(9), 2490-2499.


Cite as: http://hdl.handle.net/11858/00-001M-0000-002B-9613-9
Abstract
Activation of resting T cells usually leads to their proliferation and differentiation into effector cells and a subsequent decline following elimination of the antigen. A situation of excessive antigen density may result in T cell receptor (TCR)-induced deletion of T effector cells, a process termed antigen-induced cell death (AgICD). Previous studies indicate that AgICD of cytotoxic T cells may be induced by either of the two key cytotoxic processes, granule exocytosis, including perforin and granzymes, or the Fas ligand (FasL)/Fas pathway. By using in vitro-polyclonally activated or ex vivo-derived virus-induced T cell populations from mice with mutations or targeted gene defects in one or more components of the two key cytolytic pathways we now show that TCR-induced apoptosis is only impaired in the absence of FasL and/or Fas, but not in the absence of perforin and/or granzymes. Furthermore, antibody-blockage of FasL alone is sufficient to inhibit early T cell death. Inhibition of both, FasL and tumor necrosis factor (TNF-α) is required to abrogate late apoptosis by AgICD. The fact that antibodies to IFN-γ also inhibit AgICD suggests that the perforin plus granzyme-independent and FaSL and/or TNF-α facilitated process of AgICD of T effector cells is tightly regulated by endogenous IFN-γ.