摘要目的:分析IgA肾病（IgAN）伴扁桃体炎患者辅助T细胞22（Th22）细胞及相关细胞因子、趋化因子轴的表达变化，探讨其与临床病理改变的关系。方法:纳入2015年6月至2016年6月在中南大学湘雅医院经肾活检确诊为IgAN的患者为研究对象。按照肾脏病理类型及是否合并扁桃体炎分为IgAN合并扁桃体炎（IgAN+扁桃体炎）组、单纯IgAN（IgAN）组、系膜增生性肾小球肾炎（MsPGN）组和对照组（HC）组。采用流式细胞术检测外周血Th17、Th22细胞及Th22细胞CC型趋化因子受体（CCR）4、CCR6、CCR10表达阳性细胞占比；酶联免疫吸附法（ELISA）检测Th22细胞效应因子白细胞介素（IL）-22，促分化因子IL-1β、IL-6、TNF-α、CC型趋化因子配体（CCL）22、CCL20、CCL27水平。免疫组织化学方法（IHC）检测肾组织中CCL22、CCL20和CCL27的表达。比较分析各组临床病理指标、Th22细胞占比及相关趋化因子表达的差异。结果:本研究共纳入44例IgAN患者，其中14例合并扁桃体炎，另纳入10例MsPGN患者及16例健康人作为对照。各组性别、年龄匹配，血压、肾功能、血脂等生化指标的差异无统计学意义（均 P>0.05）。IgAN组、MsPGN组及IgAN+扁桃体炎组外周血Th22细胞、CCR10表达阳性细胞占比明显高于对照组，血清IL-22、IL-1β、IL-6、TNF-α、CCL20、CCL22、CCL27水平亦较高，且IgAN+扁桃体炎组更为显著（均 P<0.05）。各组肾脏组织CCL20、CCL22、CCL27表达改变与其外周血变化一致。合并血尿的IgAN患者外周血Th22细胞占比显著高于无血尿组患者。病理分型（E1、S1或T1-2）较重的IgAN患者外周血Th22细胞占比显著高于病理分型较轻者（E0、S0或T0）。 结论:Th22细胞及CCL27/CCR10轴参与了IgAN发病过程，扁桃体炎可加重IgAN的临床与病理损伤。

abstractsObjective:To analyze the changes of helper T cell 22 (Th22) and related cytokines and chemokines in patients with IgA nephropathy (IgAN) and tonsillitis, and explore its relationship with clinical pathological changes.Methods:IgAN patients who were diagnosed at the Xiangya Hospital of Central South University from June 2015 to June 2016 were included. They were divided into IgAN and tonsillitis (IgAN+tonsillitis) group, IgAN group, mesangial proliferative glomerulonephritis (MsPGN) group and control group (HC) group according to renal pathology and whether associated with tonsillitis. Flow cytometry was used to detect the percentage of peripheral blood Th17, Th22 cells, CC-type chemokine receptor (CCR) 4, CCR6 and CCR10 cells. Enzyme-linked immunosorbent assay (ELISA) was used to detect the levels of interleukin (IL)-22, IL-1β, IL-6, TNF-α, CCL22, CCL20 and CCL27. Immunohistochemical method (IHC) was used to detect the expression of CCL22, CCL20 and CCL27 in kidney tissue. The differences of clinicopathological indicators, the proportion of Th22 cells and related chemokine in each group were compared and analyzed.Results:A total of 44 IgAN patients were included, including 14 patients complicated with tonsillitis. Ten MsPGN patients and 16 healthy people were also included. There was no statistically significant difference in gender, age, blood pressure, kidney function, blood lipid and other biochemical indicators among the groups (all P>0.05). The peripheral blood Th22 cells and CCR10 positive cells in the IgAN group, MsPGN group, and IgAN+tonsillitis group were significantly higher than those of the control group, and serum IL-22, IL-1β, IL-6, TNF-α, CCL20, CCL22 and CCL27 levels were also significantly higher (all P<0.05). All above indexes reached the highest levels in IgAN patients combined with tonsillitis. The changes of CCL20, CCL22 and CCL27 in renal tissues were consistent with those in peripheral blood. The percentage of Th22 cells increased in hematuria-positive and higher MEST scores patients. Conclusions:Th22 cells cooperated with CCL27/CCR10 axis are involved in the pathogenesis of IgAN. Tonsillitis exacerbates clinical severity and kidney injury of IgAN.