Cbx3/HP1 gamma is a histone reader whose function in the immune system is not completely understood. Here, we demonstrate that in CD8(+) T cells, Cbx3/HP1. insufficiency leads to chromatin remodeling accompanied by enhanced Prf1, Gzmb and Ifng expression. In tumors obtained from Cbx3/HP1 gamma-insufficient mice or wild type mice treated with Cbx3/HP1 gamma-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/HP1 gamma-insufficient mice or wild type mice treated with Cbx3/HP1 gamma-insufficient CD8(+) T cells. These findings suggest that targeting Cbx3/HP1. can represent a rational therapeutic approach to control growth of solid tumors.
Cbx3/HP1 gamma deficiency confers enhanced tumor-killing capacity on CD8(+) T cells
Creators
Michael Sun - Beth Israel Deaconess Medical Center
Ngoc Ha - Drexel University
Duc-Hung Pham - Beth Israel Deaconess Medical Center
Megan Frederick - Scripps Research Institute
Bandana Sharma - Dana-Farber Cancer Institute
Chie Naruse - Kyoto University
Masahide Asano - Kyoto University
Matthew E. Pipkin - Scripps Research Institute
Rani E. George - Harvard University
To-Ha Thai - Beth Israel Deaconess Medical Center
Publication Details
Scientific reports, Vol.7(1), pp.42888-42888
Publisher
Springer Nature
Number of pages
12
Grant note
R21CA198263 / NATIONAL CANCER INSTITUTE; United States Department of Health & Human Services; National Institutes of Health (NIH) - USA; NIH National Cancer Institute (NCI)
Friends for Life Research Grant
AI099012 / NIH-NIAID grant
Mayer Family Fund
Resource Type
Journal article
Language
English
Academic Unit
Neurobiology and Anatomy
Identifiers
991019167832304721
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Web of Science research areas
Multidisciplinary Sciences
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