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

• DOI: 10.1126/science.aah6499
• Publication Date: 2018-01-16T22:40:52Z
• Authors: Luigia Pace; Christel Goudot; Elina Zueva; Paul Gueguen; Nina Burgdorf; Joshua J. Waterfall; Jean-Pierre Quivy; Geneviève Almouzni; Sebastian Amigorena
• Keywords: 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

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