| First Author | Zhao H | Year | 2001 |
| Journal | J Exp Med | Volume | 194 |
| Issue | 10 | Pages | 1441-8 |
| PubMed ID | 11714751 | Mgi Jnum | J:72761 |
| Mgi Id | MGI:2153566 | Doi | 10.1084/jem.194.10.1441 |
| Citation | Zhao H, et al. (2001) Impaired c-Jun Amino Terminal Kinase Activity and T Cell Differentiation in Death Receptor 6-deficient Mice. J Exp Med 194(10):1441-8 |
| abstractText | During an immune response naive T helper (Th) cells differentiate into two functionally distinct subsets, Th1 and Th2, based on their cytokine secretion profile and immunomodulatory function. c-Jun amino terminal kinase (JNK) regulates Th cell differentiation by activating a transcriptional program required for cytokine production. We have recently identified a TNFR superfamily death domain-containing molecule, death receptor (DR)6, which potently activates JNK. T cells from DR6-deficient mice are substantially impaired in JNK activation. When DR6(-/-) mice were challenged with protein antigen, their T cells hyperproliferate and display a profound polarization toward a Th2 response whereas Th1 differentiation is not equivalently affected. In addition, DR6(-/)- T cells showed preference toward Th2 differentiation in vitro. The phenotype seen in the DR6(-/)- mice is not due to the apoptotic pathway. Therefore, DR6, working through JNK, rather than apoptosis, functions to attenuate the Th2 response. This is the first demonstration of a role in the activation and differentiation of Th cells by DR6 in particular and DRs in general. |
