IgA肾病（IgAN）是难治性肾小球疾病，发病机制尚未明确。近年研究提示IgAN存在Th17/Treg失衡，是重要致病因素之一。髓系抑制细胞（MDSC）是骨髓来源前体细胞，在多种自身免疫疾病中参与免疫应答。我们前期已证明MDSC在SLE患者及人源化SLE小鼠中有促Th17分化及致病作用。我们近期发现IgAN患者外周血中MDSC显著增多，且存在Th17/Treg失衡。STAT3通路是Th17、Treg分化交叉点，炎性条件下该通路可诱导Th17/Treg失衡。我们推测，IgAN中MDSC分泌炎性因子，通过STAT3通路影响Th17和Treg的分化，诱导Th17/Treg失衡。因此本项目拟利用IgAN患者外周血、IgAN小鼠模型及体外Th17、Treg分化体系，从分子、细胞、动物及患者多方面分析，研究IgAN中MDSC对Th17和Treg分化的影响，确认其作用机制，为临床治疗IgAN提供新靶点。

IgA nephropathy (IgAN) is one kind of refractory glomerular diseases. At present, the pathogenesis of IgAN is still unclear. Recent studies have suggested that there is a Th17/Treg imbalance in IgAN, which is one of the pathogenic factors. Myeloid-derived suppressor cells (MDSC) are heterogeneous population of immature cells derived from myeloid progenitors, which are accumulated in a variety of autoimmune diseases and participate in immune responses. Our preliminary data showed that MDSC have the roles of promoting Th17 differentiation and disease progression in SLE patients and humanized SLE mice. Meanwhile, we found MDSC were significantly amplified in IgAN patients, and there is a Th17/Treg imbalance in the blood of IgA patients. STAT3 pathway is the cross point of Th17 and Treg differentiation. Under inflammatory conditions, the pathway can induce the imbalance of Th17/Treg. Therefore, we put forward the following hypothesis: in the inflammatory condition of IgA nephropathy, MDSC can secrete pro-inflammatory cytokines and affect the differentiation of Th17 cells and Treg cells through STAT3 pathway, resulting in imbalance of Th17/Treg cells and promoting renal tissue injury. Based on the above hypothesis, we will investigate the effect of MDSC on Th17 and Treg differentiation by using the Th17 and Treg differentiation system in vitro, clinical samples from IgAN patients and IgAN mouse model. We aim to make clear the effect and the possible mechanism of MDSC in IgAN. This study will provide us new reference for clinical prognosis and new targets for clinical therapy.