复发性宫颈癌严重危害女性健康，目前尚无有效治疗方法。我们前期研究显示，经宫颈阴道黏膜使用HPV治疗性疫苗在局部产生了CD103+CD8+组织型记忆性T细胞（TRM）。TRM对复发性肿瘤的治疗非常有效，但诱导其产生的机制目前尚不清楚。转录因子Bcl11b在肺TRM的产生中起重要作用，我们预实验提示其与TGF-β协同作用促进CD8+T细胞中CD103的表达。因此设想Bcl11b可能通过TGF-β信号通路来调控CD103+CD8+TRM的产生和功能。为此，我们将首先研究Bcl11b对CD103+CD8+TRM生成及组织定位的影响；其次，分析Bcl11b通过TGF-β信号通路调控CD103+CD8+TRM产生的机制；再次，验证Bcl11b调控的CD103+CD8+TRM在宫颈癌复发模型中的抗肿瘤效应。本课题的研究将阐明TRM产生的新机制，为宫颈癌治疗性疫苗的研制以及复发性宫颈癌的治疗提供新的策略。

Recurrent cervical cancer is a threat to women’s health, and current therapies for this disease are not effective. Our previous studies have shown that intravaginal adiministration of HPV vaccine can produce CD103+CD8+TRM in the cervicovaginal tract. TRM is very effective in the treatment of recurrent tumors, but the mechanisms of its generation are not clear. Transcriptional factor Bcl11b plays an important role in the generation of TRM in the lung. We have preliminary data demostrate that Bcl11b can cooperate with TGF-β signal pathway to promote exprssion of CD103 in CD8+ T cells. Therefore, we assume that Bcl11b may control the production and function of CD103+CD8+TRM through the TGF-β signal pathway. To this end, we will focus on the following studies:① we will study the influence of Bcl11b on CD103+CD8+TRM generation and tissue localization; ② we will discuss the mechanisms that Bcl11b regulates CD103+CD8+TRM generation through TGF-β signal pathway; ③ we will verificate the anti-tumor effect of CD103+CD8+TRM regulated by Bcl11b in recurrent cervical cancer model. Our study will clarify the new mechanisms of TRM generation and provide a new strategy for the design of therapeutic cervical cancer vaccine and the treatment of reccurent cervical cancer.