免疫治疗成为三阴性乳腺癌（triple-negative breast cancer，TNBC）新的具有前景的治疗手段。肿瘤局部CD8+T细胞浸润对TNBC免疫治疗发挥疗效至关重要。我们研究发现，Med19是乳腺癌中癌基因，且与肿瘤中CD8A负相关。抑制Med19表达，芯片结果显示趋化因子CXCL11表达升高，CXCL11被报道通过促进CD8+T细胞浸润发挥抗肿瘤作用。抑制Med19表达，TNBC细胞对CD8+T细胞杀伤作用敏感性增强，我们推测Med19可能通过调控CXCL11表达影响TNBC中CD8+T细胞免疫浸润。通过Co-IP和质谱分析鉴定Med19相互作用分子，进一步探究Med19调控CXCL11的机制。本项目拟从细胞、动物以及临床样本水平进一步阐明Med19作用机制，有望揭示Med19调控CXCL11影响TNBC中CD8+T免疫浸润机制，为TNBC免疫治疗提供新的分子靶点。

Immunotherapy has become a promising new treatment for triple-negative breast cancer (TNBC). Intratumor CD8+ T cell infiltration is essential for TNBC immunotherapy. We found that Med19 was an oncogene in breast cancer and negatively correlated with CD8A expression. After knockdown Med19 expression in TNBC cells, the microarray results showed that chemokine CXCL11 expression was increased, which has been reported to play an anti-tumor role in promoting the infiltration of CD8+ T cells. Furthermore, inhibition of Med19 expression increased the sensitivity of TNBC cells to CD8+ T cells killing effect. We speculated that Med19 may affect CD8+ T cells immune infiltration in TNBC through regulating the expression of CXCL11. To explore the potential mechanism of Med19 in regulating CXCL11, we performed Co-IP and mass spectrometry to identify the molecules interacting with Med19. In this project, we will further clarify the mechanism of Med19 in cells, animal model and TNBC patient tissues. This study is expected to illustrate the mechanism of Med19 in regulating CXCL11 to affect CD8+ T cells immune infiltration in TNBC and provide a potential target for TNBC immunotherapy.