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GADD45gamma mediates the activation of the p38 and JNK MAP kinase pathways and cytokine production in effector TH1 cells.

Abstract：

:The p38 and JNK stress-activated MAPK signal transduction pathways are activated by T cell receptor (TCR) signaling and are required for IFN-gamma production by TH1 effector cells. Here, we show that the expression of GADD45gamma is induced during T cell activation and that the level of expression is higher in TH1 cells than in TH2 cells. TH1 cells from GADD45gamma(-/-) mice are severely compromised in their abilities to activate p38 and JNK in response to TCR signaling, produce much less IFN-gamma upon restimulation, and are deficient in activation-induced cell death (AICD). Additionally, GADD45gamma deficiencies caused reduced contact hypersensitivity in mice. Thus, GADD45gamma mediates activation of the p38 and JNK pathways and effector function of TH1 cells.

journal_name

Immunity

journal_title

Immunity

authors

Lu B,Yu H,Chow C,Li B,Zheng W,Davis RJ,Flavell RA

doi

10.1016/s1074-7613(01)00141-8

keywords:

subject

Has Abstract

pub_date

2001-05-01 00:00:00

pages

583-90

issue

5

eissn

1074-7613

issn

1097-4180

pii

S1074-7613(01)00141-8

journal_volume

14

pub_type

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