| First Author | Tao J | Year | 2007 |
| Journal | Eur J Immunol | Volume | 37 |
| Issue | 3 | Pages | 818-29 |
| PubMed ID | 17301952 | Mgi Jnum | J:118685 |
| Mgi Id | MGI:3700105 | Doi | 10.1002/eji.200636726 |
| Citation | Tao J, et al. (2007) JNK2 negatively regulates CD8(+) T cell effector function and anti-tumor immune response. Eur J Immunol 37(3):818-29 |
| abstractText | JNK1 and JNK2 have distinct effects on activation, differentiation and function of CD8(+ )T cells. Our early studies demonstrated that JNK1 is required for CD8(+) T cell-mediated tumor immune surveillance. However, the role of JNK2 in CD8(+) T cell response and effector functions, especially in anti-tumor immune response, is unknown. To define the role of JNK2 in antigen-specific immune response, we have investigated CD8(+) T cells from OT-1 CD8(+) transgenic mice in response to either high- or low-affinity peptides. JNK2(-/-) CD8(+) T cells proliferated better in response to both peptides, with more cell division and less cell death. In addition, JNK2(-/-) CD8(+) T cells produced higher levels of IFN-gamma, which is associated with increased expression of T-bet and Eomesodermin (Eomes). Moreover, JNK2(-/-) CD8(+) T cells expresses high levels of granzyme B and show increased CTL activity. Finally, the enhanced expansion and effector function of JNK2(-/-) CD8(+ )T cells was further evidenced by their capacity to delay tumor growth in vivo. In summary, our results demonstrate that JNK2 negatively regulates antigen-specific CD8(+) T cell expansion and effector function, and thus selectively blocking JNK2 in CD8(+) T cells may potentially enhance anti-tumor immune response. |
