间质纤维化是机体通过调节肿瘤微环境从而影响其发生发展的重要途径，肿瘤局部慢性炎症与间质纤维化同时存在、相互促进，但机制未明。调节性B细胞Bregs是B细胞的特殊亚群，以分泌IL-10为特征，可调控T细胞增殖分化。我们前期研究发现，舌鳞癌细胞通过肿瘤源性Foxp3调控TGF-β，在微环境中与Tregs细胞对话，使微环境向Tregs偏移，诱导免疫抑制，但与"Tregs-Th17"微环境存在差异；进一步研究发现，舌鳞癌IL-10表达上升，存在CD19+淋巴细胞浸润，提示Bregs可能在舌鳞癌微环境中发挥作用。据此我们率先提出，Bregs通过影响Tregs-Th17炎性微环境调控舌鳞癌间质纤维化。拟首先分析间质纤维化对舌鳞癌发生发展的影响，然后在信号通路、细胞因子网络、细胞接触作用、基因敲除小鼠等水平阐明Bregs在舌鳞癌炎性微环境与间质纤维化之间的调控机制，为舌鳞癌生物治疗提供实验及理论依据。

Interstitial fibrosis contributes to tumor progression by its dynamic regulation with chronic inflammation in tumor microenvironment. Regulatory B cells (Bregs), characterized by IL-10 secretion, is a special subpopulation of B cells, and they are reported to function in T cells proliferation and differentiation. Our previous study revealed that tongue squamous cell carcinoma (TSCC) cells expressed tumor-originated Foxp3, and that tumor-originated Foxp3 cross-talked with Foxp3+ Tregs via TGF-β to induce immunosuppression in vitro, which, however, contradicted to "Tregs-Th17" microenvironment in vivo. Then our study showed IL-10 expression was up-regulated and CD19+ lymphocytes existed in TSCC tissues, which indicated that Bregs may function in TSCC inflammatory microenvironment. Based on studies above, we propose that Bregs regulate interstitial fibrosis by regulating Th17-Tregs inflammatory microenvironment in TSCC. We will at first analyze the association between interstitial fibrosis and TSCC clinipathologic features, and then investigate regulation mechanisms between Bregs, Tregs, Th17 and interstitial fibrosis in vitro and in vivo. We hope this study will illustrate a new theory in inflammatory microenvironment and interstitial fibrosis regulation.