我们以前研究证实Akt2通过FoxO-1-ICOS轴调控NKT17细胞的发育和功能，Akt2反馈调控ICOS的表达。前期发现CD23在iNKT细胞中表达，CD23缺失导致iNKT细胞和NKT17亚群的数量降低，IL-17的分泌减少，但是CD23如何调控NKT17细胞分化的机制尚属未知。另外，我们发现CD23通过促进Akt2活化上调ICOS的表达，但CD23如何促进Akt2活化的分子机制和是否通过Akt2-ICOS调控NKT17细胞的分化尚属未知。本课题拟通过生化方法寻找介于CD23和Akt2上游激酶的中间分子和细胞免疫学方法证实CD23通过Akt2-ICOS调控NKT17细胞的分化。本课题将为iNKT细胞的免疫调控机制提供新思路，丰富iNKT细胞发育和功能的理论。鉴于中性粒细胞性哮喘与iNKT细胞产生的IL-17密切相关，本研究可能为iNKT细胞作为干预靶标治疗中性粒细胞性哮喘提供新策略。

Our previous studies have shown that Akt2 regulates the development and function of NKT17 cells via FoxO-1-ICOS axis, and Akt2 regulates the expression of ICOS with feedback. Previous researches have revealed that CD23 is expressed on iNKT cells, and the deficiency of CD23 results in decreased number of iNKT cells and NKT17 cells, as well as reduced secretion of IL-17. At present, how CD23 regulates the differentiation of NKT17 cells is still unclear. Also, we have found that CD23 can promote the expression of ICOS by up-regulating the activation of Akt2. However, the molecular mechanism that how CD23 promotes the activation of Akt2 and whether CD23 regulates the differentiation of NKT17 cells through Akt2-ICOS is still unknown. This study aims to find an intermediate molecule between CD23 and Akt2 upstream kinases using biochemical methods and to verify that CD23 regulates the differentiation of NKT17 cells via Akt2-ICOS by using cellular immunological methods. This research will provide new ideas for the immune regulation mechanism of iNKT cells and enrich the theory of development and function of iNKT cells. Given the importance of iNKT cells in the neutrophil asthma，which is closely related to IL-17 produced by iNKT cells, this study may also provide a new strategy for treating neutrophilic asthma with iNKT cells as intervention targets.