Title
GADD45γ Mediates the Activation of the p38 and JNK MAP Kinase Pathways and Cytokine Production in Effector TH1 Cells
Document Type
Article
Publication Date
5-2001
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.
Recommended Citation
Lu, B., Yu, H., Chow, C. W., Li, B., Zheng, W. P., Davis, R. J., & Flavell, R. A. (2001). GADD45y mediates the activation of the p38 and JNK MAP kinase pathways and cytokine production in effector T(H)1 Cells. Immunity, 14(5), 583-590.
Comments
This article first appeared in the May 2001 issue of Immunity and is linked to with permission.
Copyright © 2001 Cell Press. All rights reserved.