Treg细胞功能降低是类风关发病的重要机制。本课题组前期研究发现FOXP3磷酸化修饰增强Treg细胞功能，类风关中FOXP3磷酸化水平减少与Treg细胞功能降低有关，类风关中蛋白激酶PKCa表达与活性降低。但FOXP3磷酸化位点，特异性蛋白激酶及其和类风关中Treg细胞功能关系尚不清楚。本课题拟从三方面展开研究:① FOXP3磷酸化位点的确定以及特异性磷酸化抗体制备；②FOXP3磷酸化蛋白激酶PKCa的确立与Treg细胞功能关系。③类风关中PKCa与Treg细胞功能降低的关系。课题创新点在于：①首次探索FOXP3磷酸化位点及制备特异性磷酸化抗体。②首次研究FOXP3磷酸化蛋白激酶PKCa与Treg细胞功能的关系及在类风关中的作用。研究结果将从PKCa和FOXP3磷酸化水平新视点阐明类风关中Treg细胞功能降低的分子机制，有助于拓展类风关发病机制，为免疫治疗提供新的理论基础与靶点。

Regulatory T (Treg) cells play a critical role in keeping autoimmunity in check, and impaired Treg cell function is associated with autoimmune pathology of rheumatoid arthritis (RA). In the previous study, we found that FOXP3 phosphorylation enhanced Treg cells function, but FOXP3 phosphorylation and Treg function were decreased in the activated RA patients. Also, the expression level and activity of protein kinase C-alpha (PKCa) reduced in the activated RA patients. However,FOXP3 phosphorylation site, the specific protein kinase and the relationship with Treg function in RA needs to be further investigated. Here we want to study the project from three aspects:① Identification of the FOXP3 phosphorylation site and prepared the specific phosphorylation antibody. ②Identification of the FOXP3 specific protein kinase PKCa and explore the relationship with Treg function. ③ The role of PKCa in the impaird function of Treg cells in RA patients. The innovation of the study is that first to explore the FOXP3 phosphorylation sites and prepare the FOXP3 specific phosphorylated antibody; first to research the role of FOXP3 specific protein kinase PKCa in the function of Treg cells of RA patients. This study will reveal a novel mechanism in which PKCa regulates FOXP3 phosphorylation, thereby altering the Treg function and provide a new theoretical basis and targets for immunotherapty of rheumatoid arthritis.