Down-regulation of IL-2 receptor α (CD25) characterizes human γδ-T cells rendered resistant to apoptosis after CD2 engagement in the presence of IL-12

B. L. Guo, K. A. Hollmig, R. D. Lopez

Research output: Contribution to journalArticle

15 Scopus citations


We recently identified a CD2-mediated, IL-12-dependent signaling pathway that inhibits apoptosis in mitogen-stimulated human γδ-T cells. Here we show that γδ-T cells which acquire resistance to mitogen-induced apoptosis upregulate IL-12 receptor beta 1 subunit (IL-12Rβ1); in contrast, γδ-T cells which remain sensitive to mitogen-induced apoptosis fail to express IL-12Rβ1. Next we show that γδ-T cells which are rendered resistant to mitogen-induced apoptosis attenuate their expression of the IL-2 receptor α chain (IL-2Rα/CD25), this in part accounting for their acquired resistance to IL-2-induced death. In contrast, apoptosissensitive γδ-T cells are shown to persist in their expression of IL-2Rα/CD25, thus remaining sensitive to IL-2-induced death. Moreover, we show that apoptosisresistant, but not apoptosis-sensitive, γδ-T cells display an enhanced responsiveness to IL-15, a finding in keeping with the known function of IL-15 as a growth and survival factor. Finally, we present evidence to suggest that this differential responsiveness to IL-15 occurs in part by the increased expression of the IL-15Rα chain on apoptosis-resistant γδ-T cells, compared to apoptosis-sensitive γδ-T cells. The biological and clinical implications of these findings are discussed.

Original languageEnglish (US)
Pages (from-to)625-637
Number of pages13
JournalCancer Immunology, Immunotherapy
Issue number11
StatePublished - Jan 2002



  • IL-15
  • IL-2 receptor
  • Immunotherapy
  • γδ-T cells

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Oncology
  • Cancer Research

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