Gadd45β is important for perpetuating cognate and inflammatory signals in T cells
| Autor: | Anthony F. Ferrandino, Binfeng Lu, Richard A. Flavell |
|---|---|
| Rok vydání: | 2003 |
| Předmět: |
CD4-Positive T-Lymphocytes
Male MAP Kinase Kinase 4 Receptors Antigen T-Cell alpha-beta Immunology Biology Lymphocyte Activation p38 Mitogen-Activated Protein Kinases CCL5 Mice Interleukin 21 Animals Immunology and Allergy Cytotoxic T cell IL-2 receptor Antigen-presenting cell Mice Knockout Mitogen-Activated Protein Kinase Kinases ZAP70 JNK Mitogen-Activated Protein Kinases CD28 Th1 Cells Natural killer T cell Antigens Differentiation Immunity Innate Cell biology Enzyme Activation Cytokines Female Mitogen-Activated Protein Kinases Carrier Proteins Signal Transduction |
| Zdroj: | Nature Immunology. 5:38-44 |
| ISSN: | 1529-2916 1529-2908 |
| DOI: | 10.1038/ni1020 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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