IL-36γ promotes antitumor immune responses (TUM10P.1028)

• Published in: The Journal of immunology (1950) 2015-05, Vol.194 (1_Supplement), p.211-211.9
• Main Authors: zuo, shuting, Wang, Xuefeng, Lu, Binfeng
• Format: Article
• Language: English
• ISSN: 0022-1767; 1550-6606
• DOI: 10.4049/jimmunol.194.Supp.211.9

Introduction of an appropriate inflammation to tumor should greatly increase tumor immunogenicity and thereby help breaking immune tolerance to tumor antigens and increase response rates of immunotherapy. Cytokines play a pivotal role in regulating tumor immunogenicity and antitumor immunity. IL-36γ is important for the IL-23/IL-17-dominated autoimmune diseases as well as anti-BCG Th1 immune responses. However, the impact of IL-36γ on tumor immunity is unknown. Here, we found IL-36γ stimulated IFN-γ production by CD8 T cells synergistically with TCR signaling and/or IL-12. Importantly, IL-36γ exerted profound antitumor effects in vivo and transformed the tumor microenvironment in favor of tumor eradication. Furthermore, IL-36γ strongly increased the efficacy of tumor vaccination. Our work also showed that IL-36γ expression in human cancers inversely correlated with cancer progression. Our study establishes a novel role of IL-36γ in promoting antitumor immune responses and suggests its potential clinical translation in cancer immunotherapy.