| First Author | Lu B | Year | 2004 |
| Journal | Nat Immunol | Volume | 5 |
| Issue | 1 | Pages | 38-44 |
| PubMed ID | 14691480 | Mgi Jnum | J:87396 |
| Mgi Id | MGI:2686819 | Doi | 10.1038/ni1020 |
| Citation | Lu B, et al. (2004) Gadd45beta is important for perpetuating cognate and inflammatory signals in T cells. Nat Immunol 5(1):38-44 |
| abstractText | 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. |
