由于肿瘤微环境中TILs处于免疫抑制状态，难以发挥有效的免疫应答作用，寻找合适的手段恢复和激活TILs的免疫功能，是开辟肿瘤免疫治疗的有效途径。.本项目拟通过体外分析IL-33促进I型淋巴细胞（包括CD8+ T、NK和γδT）活化、增殖的效应与机制，研究在肺鳞癌动物模型体内IL-33介导激活TILs的效应与机制，证实IL-33在肿瘤免疫治疗中的功能，并探讨IL-33在人肺鳞癌微环境中的表达及其临床意义，来阐明IL-33通过激活TILs介导抗肿瘤免疫应答的功能与机制，揭示其运用于肺鳞癌免疫治疗的潜在价值，为临床免疫治疗肺鳞癌肿瘤开辟新的途径。

The tumor infiltrating lymphocytes (TILs) cannot exert effective antitumor immune responses due to their suppression by kinds of inhibitory mechanisms. Hence, it’s a promising pathway of cancer therapy through activating TILs by appropriate stimulus. This project aims to explore the function and mechanism of IL-33 on activating TILs and antitumor responses. Our plan is as follows: (1) Investigating the effect and mechanism of IL-33 on activating CD8+ T、NK and γδT cells in vitro. (2) Identifying IL-33 can promote type 1 lymphocyte-mediated antitumor immune responses in vivo. (3) Exposing the correlation of IL-33 expression with clinical parameters. (4) Exploring the function of IL-33 on cancer therapy.

由于肿瘤微环境中TILs处于免疫抑制状态，难以发挥有效的免疫应答作用，寻找合适的手段恢复和激活TILs的免疫功能，是开辟肿瘤免疫治疗的有效途径。本项目通过体外分析证实IL-33促进TILs活化、增殖，并阐明IL-33通过激活PI3K/Akt/mTORC1途径介导对CD8+T细胞功能的促进作用；通过体内动物实验证实IL-33促进肿瘤微环境中CD4+TILs和CD8+TILs的数量，并与肿瘤进展呈负相关。