Gadd45[beta] is important for perpetuating cognate and inflammatory signals in T cells

Gadd45beta (growth arrest and DNA damage-inducible, beta) is involved in cell cycle arrest, apoptosis, signal transduction and cell survival. In T cells, Gadd45b was rapidly induced by T cell receptor (TCR) and inflammatory signals. Deficiency of Gadd45beta in CD4+ T cells impaired their responses t...

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Published inNature immunology Vol. 5; no. 1; pp. 38 - 44
Main Authors Lu, Binfeng, Ferrandino, Anthony F, Flavell, Richard A
Format Journal Article
LanguageEnglish
Published New York Nature Publishing Group 01.01.2004
Subjects
Deoxyribonucleic acid
DNA
ERK protein
Gadd45 gene
JNK protein
Listeria monocytogenes
p38 protein
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Summary:Gadd45beta (growth arrest and DNA damage-inducible, beta) is involved in cell cycle arrest, apoptosis, signal transduction and cell survival. In T cells, Gadd45b was rapidly induced by T cell receptor (TCR) and inflammatory signals. Deficiency of Gadd45beta in CD4+ T cells impaired their responses to TCR stimulation or inflammatory cytokines. ERK, p38 and JNK activation were all substantially suppressed in Gadd45beta-deficient CD4+ T cells. Cytokine production by Gadd45beta-deficient CD4+ T cells was also impaired. Furthermore, Gadd45beta mediated inflammatory cytokine production by dendritic cells, and Gadd45beta-deficient mice showed an impaired T helper type 1 response during Listeria monocytogenes infection. Gadd45beta is therefore a critical feedback regulator that perpetuates both cognate and inflammatory signals.
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ISSN:1529-2908
1529-2916
DOI:10.1038/ni1020