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

Nat Immunol. 2022 Feb;23(2):262-274. doi: 10.1038/s41590-021-01120-y. Epub 2022 Jan 31.


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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • CD4-Positive T-Lymphocytes / immunology
  • CD8-Positive T-Lymphocytes / immunology
  • Cell Line, Tumor
  • Cytokines / immunology
  • Female
  • Humans
  • Immune Checkpoint Inhibitors / immunology
  • Immunity, Innate / immunology*
  • Lymphocytes / immunology*
  • Mice
  • Mice, Inbred BALB C
  • Mice, Inbred C57BL
  • Neoplasms / immunology*
  • Neoplasms / therapy*


  • Cytokines
  • Immune Checkpoint Inhibitors