MHC II作为抗原提呈分子在T细胞分化和启动适应性免疫应答过程中的重要作用一直被广泛研究，然而MHC II分子自身表达尤其是其亚基组装的分子机制至今仍不明确。微管相关蛋白1轻链3B（LC3B）是介导细胞自噬形成的重要分子。我们在前期研究中发现LC3B敲除小鼠存在CD4+ T细胞亚型和免疫细胞MHC II分子表达的缺陷，而MHC II分子α和β亚基的转录表达基本没有改变。据此我们提出本项目的关键科学假设：LC3B分子通过介导α亚基和β亚基的组装调控免疫细胞中MHC II分子的表达，而且该过程可能不依赖于细胞自噬。本项目拟通过整体动物模型和分子生物学方法探究LC3B调控MHC II分子亚基组装和CD4+ T细胞分化的机制，并通过基因组学和蛋白组学寻找LC3B调控MHC II表达的可能的协同分子。本研究预期揭示调控MHC II分子亚基组装的新机制，同时也拓展LC3B介导细胞自噬之外的新功能。

It has been widely investigated that MHC II molecules, serving for antigen presentation, play a critical role in CD4+ T cell development and in initiating the adaptive immune response, but the molecular mechanisms of MHC II molecule expression, especially the process of subunits assembly, remain unclear. Microtubule-associated protein 1 light chain 3B (LC3B) is an important molecule in the process of autophagy. We recently noticed that LC3B knockout mice exhibited deficiency of CD4+ T cells, and the MHC II expression in immune cells was also markedly decreased. Interestingly, the expression of MHC II αand βsubunits was not significantly affected. Thus, we hypothesize that LC3B orchestrate the assembly of MHC II molecules from their α and β subunits, which might be independent of autophagy. In this proposal, we will explore the molecular mechanisms of LC3B in regulation of the assembly of MHC II molecular subunits in vivo and in vitro, and will try to find out the possible synergistic molecules in this process through genomics and proteomics. This project will not only reveal a new regulatory mechanism for the expression of MHC II molecules, especially for the assembly from their subunits, but will also expand the functions of LC3B in addition to autophagic machinery.