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

The function of type 3 innate lymphoid cells (ILC3s) in cancer is still poorly understood. Bruchard et al. demonstrate that ILC3s are critical for the recruitment of T cells to the tumor microenvironment and thereby play important roles in antitumor responses. 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-1 beta 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-1 beta, which promote ILC3-dependent antitumor immunity and enhance tumor sensitivity to immunotherapy.