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Nat Immunol. 2004 Jan;5(1):38-44. Epub 2003 Dec 14.

Gadd45beta is important for perpetuating cognate and inflammatory signals in T cells.

Author information

1
Section of Immunobiology, Yale University School of Medicine, 310 Cedar Street, New Haven, Connecticut 06520-8011, USA.

Abstract

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.

PMID:
14691480
DOI:
10.1038/ni1020
[Indexed for MEDLINE]

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