The epigenetic control of stemness in CD8 + T cell fate commitment

Male Mice, Knockout [SDV]Life Sciences [q-bio] Cell Differentiation Histone-Lysine N-Methyltransferase Methyltransferases CD8-Positive T-Lymphocytes Listeria monocytogenes Methylation Chromatin Epigenesis, Genetic 3. Good health [SDV] Life Sciences [q-bio] Histones Mice, Inbred C57BL Mice 03 medical and health sciences 0302 clinical medicine Animals Female Listeriosis Gene Silencing RNA, Messenger Immunologic Memory Cells, Cultured
DOI: 10.1126/science.aah6499 Publication Date: 2018-01-16T22:40:52Z
ABSTRACT
Epigenetic modulation of effector T cells The epigenetic states and associated chromatin dynamics underlying the initiation and maintenance of memory and effector CD8 + T cells are poorly understood. Pace et al. found that mice lacking the histone H3 lysine 9 methyltransferase Suv39h1 had markedly reduced antigen-specific effector CD8 + T cell responses to Listeria monocytogenes infection (see the Perspective by Henning et al. ). Instead, CD8 + T cells in these mice were enriched for genes associated with naïve and memory signatures and showed enhanced memory potential and increased survival capacity. Thus, Suv39h1 marks chromatin through H3K9me3 deposition and silences memory and stem cell programs during the terminal differentiation of effector CD8 + T cells. Science , this issue p. 177 ; see also p. 163
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