GADD45γ mediates the activation of the p38 and JNK MAP kinase pathways and cytokine production in effector TH1 cells

Binfeng Lu, Hong Yu, Chi Wing Chow, Baiyong Li, Wei Ping Zheng, Roger J. Davis, Richard A. Flavell

Research output: Contribution to journalArticle

138 Scopus citations

Abstract

The p38 and JNK stress-activated MAPK signal transduction pathways are activated by T cell receptor (TCR) signaling and are required for IFN-γ production by TH1 effector cells. Here, we show that the expression of GADD45γ is induced during T cell activation and that the level of expression is higher in TH1 cells than in TH2 cells. TH1 cells from GADD45γ-/- mice are severely compromised in their abilities to activate p38 and JNK in response to TCR signaling, produce much less IFN-γ upon restimulation, and are deficient in activation-induced cell death (AICD). Additionally, GADD45γ deficiencies caused reduced contact hypersensitivity in mice. Thus, GADD45γ mediates activation of the p38 and JNK pathways and effector function of TH1 cells.

Original languageEnglish (US)
Article number139
Pages (from-to)583-590
Number of pages8
JournalImmunity
Volume14
Issue number5
DOIs
StatePublished - 2001

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Infectious Diseases

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    Lu, B., Yu, H., Chow, C. W., Li, B., Zheng, W. P., Davis, R. J., & Flavell, R. A. (2001). GADD45γ mediates the activation of the p38 and JNK MAP kinase pathways and cytokine production in effector TH1 cells. Immunity, 14(5), 583-590. [139]. https://doi.org/10.1016/S1074-7613(01)00141-8