Recruitment and activation of type 3 innate lymphoid cells promote antitumor immune responses.
Fiche publication
Date publication
février 2022
Journal
Nature immunology
Auteurs
Membres identifiés du Cancéropôle Est :
Dr BOIDOT Romain, Pr GHIRINGHELLI François, Pr PAUL Catherine, Mme TRUNTZER Caroline, Dr VEGRAN Frédérique, Dr REBE Cédric, Dr BRUCHARD Mélanie, Dr CHALMIN Fanny
Tous les auteurs :
Bruchard M, Geindreau M, Perrichet A, Truntzer C, Ballot E, Boidot R, Racoeur C, Barsac E, Chalmin F, Hibos C, Baranek T, Paget C, Ryffel B, Rébé C, Paul C, Végran F, Ghiringhelli F
Lien Pubmed
Résumé
Tumors poorly infiltrated by T cells are more resistant to immunogenic chemotherapies and checkpoint inhibition than highly infiltrated tumors. Using murine models, we found that CCR6 type 3 innate lymphoid cells (ILC3s) can trigger an increase in the number of T cells infiltrating a tumor. Shortly after administration of cisplatin chemotherapy, production of the chemokine CCL20 and proinflammatory cytokine IL-1β at the tumor site led to the recruitment and activation of ILC3s. Within the tumor, ILC3 production of the chemokine CXCL10 was responsible for the recruitment of CD4 and CD8 T lymphocytes to the tumor. ILC3-dependent infiltration of T cells was essential for antitumor immune responses and increased the efficacy of checkpoint inhibition. Thus, we reveal an essential role of CCL20 and IL-1β, which promote ILC3-dependent antitumor immunity and enhance tumor sensitivity to immunotherapy.
Référence
Nat Immunol. 2022 Feb;23(2):262-274