IL-17A promotes migration and tumor killing capability of B cells in esophageal squamous cell carcinoma
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Lin Lu1, Chengyin Weng1, Haibo Mao1, Xisheng Fang1, Xia Liu1, Yong Wu1, Xiaofei Cao1, Baoxiu Li1, Xiaojun Chen1, Qinquan Gan1, Jianchuan Xia2, Guolong Liu1
1Department of Medical Oncology, Guangzhou First People’s Hospital, Guangzhou Medical University, Guangzhou, 510180, China
2Department of Experimental Research and State Key Laboratory of Oncology in Southern China, Sun Yat-sen University Cancer Center, Guangzhou 510060, China
Guolong Liu, e-mail: [email protected]
Jian-chuan Xia, e-mail: [email protected]
Keywords: IL-17A, B cells, esophageal squamous cell carcinoma, recruitment, cytotoxicity
Received: July 28, 2015 Accepted: February 20, 2016 Published: March 03, 2016
We have previously reported that the accumulation of IL-17-producing cells could mediate tumor protective immunity by promoting the migration of NK cells, T cells and dendritic cells in esophageal squamous cell carcinoma (ESCC) patients. However, there were no reports concerning the effect of IL-17A on tumor infiltrating B cells. In this study, we investigated the accumulation of CD20+ B cells in the ESCC tumor nests and further addressed the effect of IL-17A on the migration and cytotoxicity of B cells. There was positive correlation between the levels of CD20+ B cells and IL-17+ cells. IL-17A could promote the ESCC tumor cells to produce more chemokines CCL2, CCL20 and CXCL13, which were associated with the migration of B cells. In addition, IL-17A enhanced the IgG-mediated antibody and complement mediated cytotoxicity of B cells against tumor cells. IL-17A-stimulated B cells gained more effective direct killing capability through enhanced expression of Granzyme B and FasL. The effect of IL-17A on the migration and cytotoxicity of B cells was IL-17A pathway dependent, which could be inhibited by IL-17A inhibitor. This study provides further understanding of the roles of IL-17A in humoral response, which may contribute to the development of novel tumor immunotherapy strategy.
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