| First Author | Lu B | Year | 2001 |
| Journal | Immunity | Volume | 14 |
| Issue | 5 | Pages | 583-90 |
| PubMed ID | 11371360 | Mgi Jnum | J:69475 |
| Mgi Id | MGI:1934710 | Doi | 10.1016/s1074-7613(01)00141-8 |
| Citation | Lu B, et al. (2001) GADD45gamma mediates the activation of the p38 and JNK MAP kinase pathways and cytokine production in effector TH1 cells. Immunity 14(5):583-90 |
| abstractText | The p38 and JNK stress-activated MAPK signal transduction pathways are activated by T cell receptor (TCR) signaling and are required for IFN-gamma production by TH1 effector cells. Here, we show that the expression of GADD45gamma is induced during T cell activation and that the level of expression is higher in TH1 cells than in TH2 cells. TH1 cells from GADD45gamma(-/-) mice are severely compromised in their abilities to activate p38 and JNK in response to TCR signaling, produce much less IFN-gamma upon restimulation, and are deficient in activation-induced cell death (AICD). Additionally, GADD45gamma deficiencies caused reduced contact hypersensitivity in mice. Thus, GADD45gamma mediates activation of the p38 and JNK pathways and effector function of TH1 cells. |
