Recruitment and activation of type 3 innate lymphoid cells promote antitumor immune responses.

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

https://www.ncbi.nlm.nih.gov/pubmed/35102345

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