Abstract
Enhancer of zeste homolog 2 (EZH2) is the catalytic subunit of polycomb repressive complex 2 (PRC2), which regulates downstream gene expression by trimethylation of lysine 27 in histone H3 (H3K27me3). EZH2 mutations or overexpressions are associated with many types of cancer. As inhibition of EZH2 activity could upregulate the expression of tumor suppressor genes, EZH2 has recently become an interesting therapeutic target for cancer therapy. Moreover, accumulating evidence has shown that EZH2 may contribute to the regulation of immune cells, especially T cells. EZH2 regulates T cell development, differentiation, and function, suggesting that EZH2 also regulates immune homeostasis in addition to tumor suppressor genes. Moreover, EZH2 can regulate T cell fate by targeting non-T cell factors such as metabolism, cytokines, and myeloid-derived suppressor cells. The role of EZH2 in this process has not been fully addressed. This review discusses up-to-date research on EZH2-mediated regulation of immunological function and the progress of immunological therapeutic strategies based on this regulation.
Highlights
Gene expression is epigenetically modified by changes in chromatin, which affects the accessibility of certain genomic loci to transcription enzymes and subsequent transcription
As the core catalytic subunit of polycomb repressive complex 2 (PRC2), Enhancer of zeste homolog 2 (EZH2) plays a crucial role in the epigenetic control of chromatin accessibility for gene transcription via histone trimethylation
This review focuses on T lymphocytes, which play an essential role in immune homeostasis
Summary
Gene expression is epigenetically modified by changes in chromatin, which affects the accessibility of certain genomic loci to transcription enzymes and subsequent transcription. In line with its function in other immune cells, EZH2 regulates the activation, proliferation, and differentiation of CD8+ T cells via histone methylation modification (Figure 2).
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