Sun, MichaelHa, NgocPham, Duc-HungFrederick, MeganSharma, BandanaNaruse, ChieAsano, MasahidePipkin, Matthew E.George, RaniThai, To-Ha2017-03-282017Sun, Michael, Ngoc Ha, Duc-Hung Pham, Megan Frederick, Bandana Sharma, Chie Naruse, Masahide Asano, Matthew E. Pipkin, Rani E. George, and To-Ha Thai. 2017. “Cbx3/HP1γ deficiency confers enhanced tumor-killing capacity on CD8+ T cells.” Scientific Reports 7 (1): 42888. doi:10.1038/srep42888. http://dx.doi.org/10.1038/srep42888.http://nrs.harvard.edu/urn-3:HUL.InstRepos:31731806Cbx3/HP1γ is a histone reader whose function in the immune system is not completely understood. Here, we demonstrate that in CD8+ T cells, Cbx3/HP1γ insufficiency leads to chromatin remodeling accompanied by enhanced Prf1, Gzmb and Ifng expression. In tumors obtained from Cbx3/HP1γ-insufficient mice or wild type mice treated with Cbx3/HP1γ-insufficient CD8+ T cells, there is an increase of CD8+ effector T cells expressing the stimulatory receptor Klrk1/NKG2D, a decrease in CD4+ CD25+ FOXP3+ regulatory T cells (Treg cells) as well as CD25+ CD4+ T cells expressing the inhibitory receptor CTLA4. Together these changes in the tumor immune environment may have mitigated tumor burden in Cbx3/HP1γ-insufficient mice or wild type mice treated with Cbx3/HP1γ-insufficient CD8+ T cells. These findings suggest that targeting Cbx3/HP1γ can represent a rational therapeutic approach to control growth of solid tumors.en-USJournal Article2017-03-2810.1038/srep42888