Chd4 choreographs self-antigen expression for central immune tolerance.


Journal

Nature immunology
ISSN: 1529-2916
Titre abrégé: Nat Immunol
Pays: United States
ID NLM: 100941354

Informations de publication

Date de publication:
08 2020
Historique:
received: 12 06 2019
accepted: 19 05 2020
pubmed: 1 7 2020
medline: 5 11 2020
entrez: 1 7 2020
Statut: ppublish

Résumé

Autoreactive T cells are eliminated in the thymus to prevent autoimmunity by promiscuous expression of tissue-restricted self-antigens in medullary thymic epithelial cells. This expression is dependent on the transcription factor Fezf2, as well as the transcriptional regulator Aire, but the entire picture of the transcriptional program has been obscure. Here, we found that the chromatin remodeler Chd4, also called Mi-2β, plays a key role in the self-antigen expression in medullary thymic epithelial cells. To maximize the diversity of self-antigen expression, Fezf2 and Aire utilized completely distinct transcriptional mechanisms, both of which were under the control of Chd4. Chd4 organized the promoter regions of Fezf2-dependent genes, while contributing to the Aire-mediated induction of self-antigens via super-enhancers. Mice deficient in Chd4 specifically in thymic epithelial cells exhibited autoimmune phenotypes, including T cell infiltration. Thus, Chd4 plays a critical role in integrating Fezf2- and Aire-mediated gene induction to establish central immune tolerance.

Identifiants

pubmed: 32601470
doi: 10.1038/s41590-020-0717-2
pii: 10.1038/s41590-020-0717-2
doi:

Substances chimiques

Autoantigens 0
CHD4 protein, human 0
Transcription Factors 0
Mi-2 Nucleosome Remodeling and Deacetylase Complex EC 3.5.1.98
Mi-2beta protein, mouse EC 3.6.1.3
DNA Helicases EC 3.6.4.-

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

892-901

Subventions

Organisme : NIGMS NIH HHS
ID : R01 GM034277
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA133404
Pays : United States
Organisme : NCI NIH HHS
ID : P01 CA042063
Pays : United States

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Auteurs

Yoshihiko Tomofuji (Y)

Department of Immunology, Graduate School of Medicine and Faculty of Medicine, The University of Tokyo, Tokyo, Japan.

Hiroyuki Takaba (H)

Department of Immunology, Graduate School of Medicine and Faculty of Medicine, The University of Tokyo, Tokyo, Japan.

Hiroshi I Suzuki (HI)

David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA, USA.
Division of Molecular Oncology, Center for Neurological Diseases and Cancer, Nagoya University Graduate School of Medicine, Nagoya, Japan.

Rayene Benlaribi (R)

Department of Immunology, Graduate School of Medicine and Faculty of Medicine, The University of Tokyo, Tokyo, Japan.

Cristian David Peña Martinez (CDP)

Department of Immunology, Graduate School of Medicine and Faculty of Medicine, The University of Tokyo, Tokyo, Japan.

Yoshihiro Abe (Y)

Department of Immunology, Graduate School of Medicine and Faculty of Medicine, The University of Tokyo, Tokyo, Japan.

Yasuyuki Morishita (Y)

Department of Molecular Pathology, Graduate School of Medicine and Faculty of Medicine, The University of Tokyo, Tokyo, Japan.

Tadashi Okamura (T)

Department of Laboratory Animal Medicine, Research Institute, National Center for Global Health and Medicine, Tokyo, Japan.
Section of Animal Models, National Center for Global Health and Medicine, Tokyo, Japan.

Akashi Taguchi (A)

Research Center for Advanced Science and Technology, The University of Tokyo, Tokyo, Japan.

Tatsuhiko Kodama (T)

Research Center for Advanced Science and Technology, The University of Tokyo, Tokyo, Japan.

Hiroshi Takayanagi (H)

Department of Immunology, Graduate School of Medicine and Faculty of Medicine, The University of Tokyo, Tokyo, Japan. takayana@m.u-tokyo.ac.jp.

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