Ligand-induced autoregulation of IFN-γ receptor β chain expression in T helper cell subsets

Erika A. Bach, Susanne J. Szabo, Anand S. Dighe, Avi Ashkenazi, Michel Aguet, Kenneth M. Murphy, Robert D. Schreiber

Research output: Contribution to journalArticle

184 Scopus citations

Abstract

Interferon γ (IFN-γ) responsiveness in certain cells depends on the state of cellular differentiation or activation. Here an in vitro developmental system was used to show that IFN-γ produced during generation of the CD4+ T helper cell type 1 (TH1) subset extinguishes expression of the cells (Fig. 3A). None of these genes guishes expression of the IFN-γ receptor β subunit, resulting in T H1 cells that are unresponsive to IFN-γ. This β chain loss also occurred in IFN-yγ-treated TH2 cells and thus represents a specific response of CD4+ T cells to IFN-γ rather than a TH1-specific Differentiation event. These results differentiation event. These results define a mechanism of cellular desensitization where a cytokine down-regulates expression of a receptor subunit required primarily for sigmammalian Ras can substitute for yeast Ras naling and not ligand binding.

Original languageEnglish
Pages (from-to)1215-1218
Number of pages4
JournalScience
Volume270
Issue number5239
DOIs
StatePublished - Jan 1 1995

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