Differential ability of T cell subsets to undergo activation-induced cell death

Arun S. Varadhachary, Somia N. Perdow, Chenggang Hu, Malini Ramanarayanan, Padmini Salgame

Research output: Contribution to journalArticlepeer-review

170 Scopus citations

Abstract

Human T cell clones were analyzed for their susceptibility to activation-induced cell death (AICD) in response to CD3/T cell receptor ligation. AICD was observed only in Th1 clones and was Fas-mediated, whereas Th2 clones resisted AICD. Analysis of a panel of Th0 clones, characterized by their ability to secrete both Th1 and Th2 cytokines, revealed that this subset included both AICD-sensitive (type A) and -resistant (type B) clones. Resistance to AICD by Th2 and Th0-type B clones was not due to lack of expression of either Fas receptor or its ligand. Paradoxically, the AICD- resistant clones were susceptible to apoptosis when Fas receptor was directly ligated by anti-Fas antibodies. However, prior activation of the resistant clones by monoclonal antibodies to CD3/TCR complex induced resistance against Fas-mediated apoptosis. Thus, the Fas-FasL pathway is critical for the induction of AICD in T cells, and moreover this pathway can be negatively regulated in the AICD-resistant clones by signals that are generated from ligation of the CD3/TCR complex.

Original languageEnglish
Pages (from-to)5778-5783
Number of pages6
JournalProceedings of the National Academy of Sciences of the United States of America
Volume94
Issue number11
DOIs
StatePublished - May 27 1997

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