Abstract
Recent studies have shown that growth arrest and DNA damage‐inducible protein 45β (Gadd45β) plays an important role in Th1 responses in the acute infectious model and promotes Th1‐mediated autoimmune diseases in experimental allergic encephalomyelitis (EAE). However, the function of Gadd45β in CD8+T cells is unclear. In this study, it is shown that Gadd45β deletion results in decreased IFNγ production and reduced levels of activated p38 MAP kinase in CD8+T cells upon TCR or IL12/IL18 stimulation. Gadd45β−/− mice are more susceptible to tumor development. The compromised CD8 T cell function caused by Gadd45b deletion is mainly responsible for the failure of tumor immunosurveillance. Taken together, our study demonstrated that Gadd45β plays an important role in tumor surveillance by promoting t tumor suppression by CD8+T cells.Grant support: Cancer Research Institute Investigator award to Binfeng Lu; Pittsburgh Cancer and Aging Program (NIH grant #P20 CA103730) to Binfeng Lu. National Natural Science Foundation of China (No. 30400394) to Songguang Ju.
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