Modulation of Fas-Dependent Apoptosis: A Dynamic Process Controlling Both the Persistence and Death of CD4 Regulatory T Cells and Effector T Cells

  • Banz A
  • Pontoux C
  • Papiernik M
106Citations
Citations of this article
23Readers
Mendeley users who have this article in their library.

Abstract

We have previously shown that regulatory CD25+CD4+ T cells are resistant to clonal deletion induced by viral superantigen in vivo. In this work we report that isolated CD25+CD4+ T cells activated in vitro by anti-CD3 Ab are resistant to Fas-induced apoptosis, in contrast to their CD25−CD4+ counterparts. Resistance of CD25+CD4+ T cells to Fas-dependent activation-induced cell death is not linked to their inability to produce IL-2 or to their ability to produce IL-10. The sensitivity of both populations to Fas-induced apoptosis can be modulated in vitro by changing the CD25+CD4+:CD25−CD4+ T cell ratio. The sensitivity of CD25−CD4+ T cells to apoptosis can be reduced, while the sensitivity of CD25+CD4+ T cells can be enhanced. Modulation of Fas-dependent apoptosis is associated with changes in cytokine production. However, while CD25−CD4+ T cell apoptosis is highly dependent on IL-2 (production of which is inhibited by CD25+CD4+ T cells in coculture), modulation of CD25+CD4+ T cell apoptosis is IL-2 independent. Taken together, these results suggest that CD25+CD4+ and CD25−CD4+ T cell sensitivity to Fas-dependent apoptosis is dynamically modulated during immune responses; this modulation appears to help maintain a permanent population of regulatory T cells required to control effector T cells.

Cite

CITATION STYLE

APA

Banz, A., Pontoux, C., & Papiernik, M. (2002). Modulation of Fas-Dependent Apoptosis: A Dynamic Process Controlling Both the Persistence and Death of CD4 Regulatory T Cells and Effector T Cells. The Journal of Immunology, 169(2), 750–757. https://doi.org/10.4049/jimmunol.169.2.750

Register to see more suggestions

Mendeley helps you to discover research relevant for your work.

Already have an account?

Save time finding and organizing research with Mendeley

Sign up for free