Publication: Cbx3/HP1γ deficiency confers enhanced tumor-killing capacity on CD8+ T cells
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Date
2017
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Nature Publishing Group
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Sun, 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.
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Abstract
Cbx3/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.
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