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T-bet is a STAT1-induced regulator of IL-12R expression in naïve CD4+ T cells

T-bet is a STAT1-induced regulator of IL-12R expression in naïve CD4+ T cells T helper type 1 (TH1) cell development involves interferon-γ (IFN-γ) signaling through signal transducer and activator of transcription 1 (STAT1) and interleukin-12 (IL-12) signaling through STAT4 activation. We examined here T-bet regulation and evaluated the actions of T-bet in STAT1- and STAT4-dependent TH1 development processes. We found that T-bet expression during T cell activation was strongly dependent on IFN-γ signaling and STAT1 activation, but was independent of STAT4. Ectopic T-bet expression strongly increased IFN-γ production in TH2 cells activated by PMA-ionomycin, but weakly increased IFN-γ production in TH2 cells stimulated by IL-12–IL-18 or OVA peptide–antigen-presenting cell stimulation. In contrast, IL-12–IL-18–induced IFN-γ production remained STAT4-dependent despite ectopic T-bet expression. Ectopic T-bet expression selectively induced expression of IL-12Rβ2, but not IL-18Rα, in wild-type and STAT1−/− TH2 cells, but did not extinguish expression of GATA-3 and TH2 cytokines. Finally, ectopic T-bet did not directly induce expression of endogenous T- bet independently of IFN-γ or STAT1. Thus, T-bet is induced by IFN-γ and STAT1 signaling during T cell activation. In addition, T-bet mediates STAT1-dependent processes of TH1 development, including the induction of IL-12Rβ2. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Nature Immunology Springer Journals

T-bet is a STAT1-induced regulator of IL-12R expression in naïve CD4+ T cells

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References (47)

Publisher
Springer Journals
Copyright
Copyright © 2002 by Nature Publishing Group
Subject
Biomedicine; Biomedicine, general; Immunology; Infectious Diseases
ISSN
1529-2908
eISSN
1529-2916
DOI
10.1038/ni794
Publisher site
See Article on Publisher Site

Abstract

T helper type 1 (TH1) cell development involves interferon-γ (IFN-γ) signaling through signal transducer and activator of transcription 1 (STAT1) and interleukin-12 (IL-12) signaling through STAT4 activation. We examined here T-bet regulation and evaluated the actions of T-bet in STAT1- and STAT4-dependent TH1 development processes. We found that T-bet expression during T cell activation was strongly dependent on IFN-γ signaling and STAT1 activation, but was independent of STAT4. Ectopic T-bet expression strongly increased IFN-γ production in TH2 cells activated by PMA-ionomycin, but weakly increased IFN-γ production in TH2 cells stimulated by IL-12–IL-18 or OVA peptide–antigen-presenting cell stimulation. In contrast, IL-12–IL-18–induced IFN-γ production remained STAT4-dependent despite ectopic T-bet expression. Ectopic T-bet expression selectively induced expression of IL-12Rβ2, but not IL-18Rα, in wild-type and STAT1−/− TH2 cells, but did not extinguish expression of GATA-3 and TH2 cytokines. Finally, ectopic T-bet did not directly induce expression of endogenous T- bet independently of IFN-γ or STAT1. Thus, T-bet is induced by IFN-γ and STAT1 signaling during T cell activation. In addition, T-bet mediates STAT1-dependent processes of TH1 development, including the induction of IL-12Rβ2.

Journal

Nature ImmunologySpringer Journals

Published: May 13, 2002

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