The “immune checkpoints”, how does it work

Titre traduit de la contribution: Les « immune checkpoints », comment ça marche

Clémence Granier, Vassili Soumelis, Marion Mandavit, Laure Gibault, Radia Belazzoug, Eléonore de Guillebon, Cécile Badoual, Eric Tartour, Hélène Roussel

Résultats de recherche: Contribution à un journalBrève enquêteRevue par des pairs

5 Citations (Scopus)

Résumé

Costimulatory molecules allow the full lymphocyte activation, whereas co-inhibitory molecules are negative counterparts that act as immune regulators, avoiding excessive response. In some context of chronic inflammation such as cancer, co-inhibitory immune checkpoint as CTLA-4, PD-1, Lag-3, Tim-3 can accumulate at the membrane of T cells leading to a state of anergy and therefore the loss of tumor growth control. Consequently, these immune checkpoints are considered as potential target in the treatment of cancer. Immunotherapy by anti-CTLA-4 and anti-PD-1/PD-L1 early demonstrated very good proof of efficacy in the setting of several cancers types, supporting the role of these molecules in tumor immune escape. The aim of this review is to summarize the pathophysiology of immune checkpoints and their therapeutic applications in cancer.

Titre traduit de la contributionLes « immune checkpoints », comment ça marche
langue originaleAnglais
Pages (de - à)18-28
Nombre de pages11
journalAnnales de Pathologie
Volume37
Numéro de publication1
Les DOIs
étatPublié - 1 févr. 2017
Modification externeOui

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