微环境的免疫状态是肿瘤免疫逃逸发生的决定因素之一。我们前期研究证实肿瘤微环境可通过多种途径促进肝癌的免疫逃逸（Oncogenesis 2016；Oncogene 2017； CDD 2018；JITC 2018），并揭示调节性B细胞是免疫逃逸的重要因素，及肝癌细胞外泌体参与调节性B细胞的分化。进一步研究发现：LncRP11-307C12.11 可显著促进肝癌细胞外泌体的释放，诱导调节性B细胞分化；上述生物学功能可能是LncRP11-307C12.11通过结合miR-138调控下游靶基因实现的。本研究拟立足前期基础，进一步系统地阐明LncRP11-307C12.11调控miR-138及其下游靶基因促进肝癌细胞外泌体释放的机制及其在调节性B细胞介导免疫逃逸中的作用。本研究不仅有助于揭示肝癌免疫逃逸的新机制，还为研制以LncRP11-307C12.11为靶点的肝癌免疫治疗提供重要理论基础。

The immune state of the microenvironment is one of the determinants of tumor immune escape. Our previous studies have confirmed that the tumor microenvironment can promote the immune escape of liver cancer through various ways (Oncogenesis 2016；Oncogene 2017； CDD 2018；JITC 2018), and revealed that regulatory B cells are important factors in immune escape, and hepatoma cell exosomes are involved in the differentiation of regulatory B cells. Further studies have found that LncRP11-307C12.11 can significantly promote the release of hepatoma cell exosomes and then induce regulatory B cell differentiation. The above biological function may be achieved by LncRP11-307C12.11 which binds to miR-138 to regulate downstream target genes. On a preliminary basis, this study intends to further systematically elucidate the mechanism by which LncRP11-307C12.11 regulates miR-138 and its downstream target genes to promote the release of hepatoma cell exosomes and its role in regulatory B cell-mediated immune escape. This study not only helps to reveal the new mechanism of immune escape of liver cancer, but also provides an important theoretical basis for the development of immunotherapy for liver cancer by targeting LncRP11-307C12.11.