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

Author:

Pace Luigia123ORCID,Goudot Christel12,Zueva Elina12,Gueguen Paul12ORCID,Burgdorf Nina12,Waterfall Joshua J.145ORCID,Quivy Jean-Pierre167ORCID,Almouzni Geneviève167ORCID,Amigorena Sebastian12ORCID

Affiliation:

1. Institut Curie, PSL Research University, F-75005 Paris, France.

2. INSERM U932, Equipes Labellisées Ligue contre le Cancer, F-75005 Paris, France.

3. Armenise-Harvard Laboratory, Italian Institute for Genomic Medicine, Turin, Italy.

4. INSERM U830, F-75005 Paris, France.

5. Institut Curie, Translational Research Department, F-75005 Paris, France.

6. CNRS, UMR3664, Equipe Labellisée Ligue contre le Cancer, F-75005 Paris, France.

7. Sorbonne Universités, UPMC University Paris 06, CNRS, UMR3664, F-75005 Paris, France.

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

Funder

H2020 European Research Council

European Research Council

Agence Nationale de la Recherche

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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