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Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
The transcription factor NFAT promotes exhaustion of activated CD8+ T Cells.
Immunity 42, 265–278 (2015)
During persistent antigen stimulation, CD8(+) T cells show a gradual decrease in effector function, referred to as exhaustion, which impairs responses in the setting of tumors and infections. Here we demonstrate that the transcription factor NFAT controls the program of T cell exhaustion. When expressed in cells, an engineered form of NFAT1 unable to interact with AP-1 transcription factors diminished T cell receptor (TCR) signaling, increased the expression of inhibitory cell surface receptors, and interfered with the ability of CD8(+) T cells to protect against Listeria infection and attenuate tumor growth in vivo. We defined the genomic regions occupied by endogenous and engineered NFAT1 in primary CD8(+) T cells and showed that genes directly induced by the engineered NFAT1 overlapped with genes expressed in exhausted CD8(+) T cells in vivo. Our data show that NFAT promotes T cell anergy and exhaustion by binding at sites that do not require cooperation with AP-1.
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Publikationstyp
Artikel: Journalartikel
Dokumenttyp
Wissenschaftlicher Artikel
Schlagwörter
Chronic Viral-infection; Regulates Pd-1 Expression; Molecular-mechanisms; Tolerance; Tim-3; Dna; Calcineurin; Proteins; Calcium; Memory
ISSN (print) / ISBN
1074-7613
e-ISSN
1097-4180
Zeitschrift
Immunity
Quellenangaben
Band: 42,
Heft: 2,
Seiten: 265–278
Verlag
Cell Press
Verlagsort
Cambridge, Mass.
Nichtpatentliteratur
Publikationen
Begutachtungsstatus
Peer reviewed
Institut(e)
Institute of Molecular Immunology (IMI)