IgA肾病患者扁桃体B1a细胞和IgA1阳性细胞表达及相关因素分析

目的 研究B1a和IgA1阳性细胞在IgA肾病患者扁桃体中的表达及B1a细胞与血尿、蛋白尿和病理Lee分级的关系。 方法 肾活检确诊为原发性IgA肾病及非肾炎慢性扁桃体炎患者各8例为对象，用免疫荧光法和激光共聚焦显微镜对其扁桃体组织进行B1a及IgA1细胞定位和定量计算，并按蛋白尿程度和Lee分级标准与IgA肾病组B1a细胞数量行统计学分析。 结果 B1a细胞主要分布在扁桃体生发中心和小结帽；IgA1细胞主要分布在上皮内、上皮下，以上皮和淋巴组织交界区为多。与慢性扁桃体炎组比较，IgA肾病组两种细胞表达明显增多（P < 0.01），且呈正相关（r = 0.778，P = 0.023）。在血尿伴蛋白尿和Lee≥Ⅲ级组B1a细胞显著高于单纯血尿和Lee<Ⅲ级组（P < 0.05）。 结论 IgA肾病患者扁桃体中IgA1可能是B1a细胞分泌的。B1a细胞数量随着患者蛋白尿的出现和病理严重程度的加重而增加，可能在疾病发生和进展过程中起着重要的作用。

Expression of B1a cells and IgA1 positive cells in tonsil of IgA nephropathy patients and analysis of associated clinicopathological factors

Objective To examine the expression of IgA1 and B1a positive cells in palatine tonsils of IgA nephropathy (IgAN) patients, and to analyze the association between B1a cells and clinicopathological changes. Methods Eight patients diagnosed as IgAN by renal biopsy and 8 chronic tonsillitis patients without nephritis as control were enrolled in the study.Immunofluorescence and laser scanning confocal microscope (LSCM) were applied to observe the localization and quantitative calculation of Bla and IgA1 positive cells. Statistic analysis of the association of B1a cells with proteinuria and pathological Lee's grading was performed. Results Bla cells were mainly localized in germinal center of tonsil, and IgA1 positive cells were mainly localized in subepithelium of tonsil. Compared to control group, the percent of B1a cells and IgA1 positive cells was significantly higher in IgAN (P＜0.01). There was a positive correlation between Bla cells and IgA1 cells (P＜0.05). In IgAN, the percent of B1a cells in patients with hematuria and proteinuria was obviously higher than that of patients with hematuria only (P＜0.05). The number of Bla cells in IgAN patients with≥Lee's grade Ⅲ was significantly higher than that of those ＜ grade Ⅲ (P＜0.05). Conclusions IgA1 may be secreted by Bla cells in the tonsil of IgAN patients. The number of B1a cells is correlated with exacerbation of proteinuria and pathological severity, which may play an important role in pathogenesis of IgAN.