T cell differentiation in chronic infection and cancer: functional adaptation or exhaustion?

Détails

ID Serval
serval:BIB_F1317F9BECF7
Type
Article: article d'un périodique ou d'un magazine.
Sous-type
Synthèse (review): revue aussi complète que possible des connaissances sur un sujet, rédigée à partir de l'analyse exhaustive des travaux publiés.
Collection
Publications
Titre
T cell differentiation in chronic infection and cancer: functional adaptation or exhaustion?
Périodique
Nature Reviews. Immunology
Auteur(s)
Speiser D.E., Utzschneider D.T., Oberle S.G., Münz C., Romero P., Zehn D.
ISSN
1474-1741 (Electronic)
ISSN-L
1474-1733
Statut éditorial
Publié
Date de publication
2014
Volume
14
Numéro
11
Pages
768-774
Langue
anglais
Notes
Publication types: Journal Article Publication Status: ppublish
Résumé
Chronic viral infections and malignant tumours induce T cells that have a reduced ability to secrete effector cytokines and have upregulated expression of the inhibitory receptor PD1 (programmed cell death protein 1). These features have so far been considered to mark terminally differentiated 'exhausted' T cells. However, several recent clinical and experimental observations indicate that phenotypically exhausted T cells can still mediate a crucial level of pathogen or tumour control. In this Opinion article, we propose that the exhausted phenotype results from a differentiation process in which T cells stably adjust their effector capacity to the needs of chronic infection. We argue that this phenotype is optimized to cause minimal tissue damage while still mediating a critical level of pathogen control. In contrast to the presently held view of functional exhaustion, this new concept better reflects the pathophysiology and clinical manifestations of persisting infections, and it provides a rationale for emerging therapies that enhance T cell activity in chronic infection and cancer by blocking inhibitory receptors.
Pubmed
Web of science
Création de la notice
27/10/2014 16:13
Dernière modification de la notice
03/03/2018 22:38
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