| First Author | Ju S | Year | 2009 |
| Journal | Eur J Immunol | Volume | 39 |
| Issue | 11 | Pages | 3010-8 |
| PubMed ID | 19688743 | Mgi Jnum | J:154199 |
| Mgi Id | MGI:4367408 | Doi | 10.1002/eji.200839154 |
| Citation | Ju S, et al. (2009) Gadd45b and Gadd45g are important for anti-tumor immune responses. Eur J Immunol 39(11):3010-3018 |
| abstractText | An effective Th1 type cell-mediated immune response against cancer cells is critical in limiting cancer progression. Gadd45b, a signaling molecule highly up-regulated during Th1 type responses, is studied for its role in limiting tumor growth. Mouse B16 melanoma cells implanted into Gadd45b(-/-) mice grew faster than those in WT or Gadd45b(+/-) littermate controls. The defect of Gadd45b(-/-) mice in tumor immunosurveillance was attributed to the reduced expression of IFN-gamma, granzyme B, and CCR5 in Gadd45b(-/-) CD8(+) T cells at the tumor site. Activation of p38 MAP kinase, but not ERK or JNK, by either TCR-stimuli or IL-12 and IL-18 is diminished in Gadd45b(-/-) CD8(+) T cells, resulting in reduced production of IFN-gamma. In addition, mRNA of T-bet and Eomes were reduced in Gadd45b(-/-) CD8(+) T cells, supporting a critical role of Gadd45b in shaping the Th1 fate. More importantly, the tumor vaccination, which is effective in WT mice, failed in Gadd45b/Gadd45g doubly deficient mice. Collectively, these data demonstrate that members of the Gadd45 gene family are important for anti-tumor immune responses. |
