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

B. Lu, H. Yu, C. W. Chow, B. Li, W. P. Zheng, R. J. Davis, R. A. Flavell

Research output: Contribution to journalArticle

136 Citations (Scopus)

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)
Pages (from-to)583-590
Number of pages8
JournalImmunity
Volume14
Issue number5
DOIs
StatePublished - 2001
Externally publishedYes

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MAP Kinase Kinase 4
p38 Mitogen-Activated Protein Kinases
Cytokines
T-Cell Antigen Receptor
MAP Kinase Signaling System
Contact Dermatitis
Signal Transduction
Cell Death
T-Lymphocytes

ASJC Scopus subject areas

  • Immunology and Allergy
  • Infectious Diseases
  • Immunology

Cite this

GADD45γ mediates the activation of the p38 and JNK MAP kinase pathways and cytokine production in effector TH1 cells. / Lu, B.; Yu, H.; Chow, C. W.; Li, B.; Zheng, W. P.; Davis, R. J.; Flavell, R. A.

In: Immunity, Vol. 14, No. 5, 2001, p. 583-590.

Research output: Contribution to journalArticle

Lu, B. ; Yu, H. ; Chow, C. W. ; Li, B. ; Zheng, W. P. ; Davis, R. J. ; Flavell, R. A. / GADD45γ mediates the activation of the p38 and JNK MAP kinase pathways and cytokine production in effector TH1 cells. In: Immunity. 2001 ; Vol. 14, No. 5. pp. 583-590.
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