IgA肾病患者淋巴细胞亚群在扁桃体组织不同部位的变化分析

The Analysis of Iymphocyte Subsets in Different Areas of Tonsil Tissues in IgA Nephropathy Patients

目的:观察IgA肾病患者与不伴肾脏疾病的慢性扁桃体炎患者CD_4、CD_(19)、CD_(20)及CD_(21)在扁桃体内的分布特点,探寻IgA肾病扁桃体生发中心及滤泡间区的淋巴细胞变化特点。方法:IgA肾病行扁桃体切除术患者33例,另15例慢性扁桃体炎行扁桃体切除术者为对照组。采用免疫组化方法检测生发中心及滤泡间区的CD_4、CD_(19)、CD_(20)及CD_(21)标记细胞数,半定量分析对比组间差异。结果:IgA肾病组扁桃体CD_4^+T细胞数无论在生发中心或滤泡间区均较对照组明显减少,滤泡间区的CD_(19)^+B细胞、CD_(20)^+B细胞、CD_(21)^+B细胞数较对照组明显增多,而生发中心内的CD_(19)^+B细胞数明显减少。结论:IgA肾病患者扁桃体内生发中心及滤泡间区的淋巴细胞分布与无肾病的慢性扁桃体炎患者存在明显差异,提示其B、T淋巴细胞的增殖、分化及聚集异常,黏膜免疫可能了参与IgA肾病发病。

Objective： To observe the distribution differences of lymphocyte subsets CD4、CD（19）、CD（20） and CD（21） in the tonsils between IgA nephropathy and tonsillitis patients without kidney disease,to explore lymphocytes change characters in germinal center and interfollicular area of the tonsils in IgA nephropathy. Methods： Thirty-three IgA nephropathy patients were under tonsillectomy,fifteen chronic tonsillitis patients with no nephropathy were treated with tonsillectomy as compare group. Immunohistochemical method was used to detect the number of CD4~＋,CD（19）~＋,CD（20）~＋ and CD（21）~＋ cells in germinal center and interfollicular area regions of tonsil tissues,and the difference was analyzed by semi-quantitative analysis. Results： The number of CD4~＋ T cells in germinal center and interfollicular area of tonsil tissues in IgA nephropathy were significantly lower than those in the control group,CD（19）~＋ B cells、CD（20）~＋ B cells and CD（21）~＋ B cells in interfollicular area were significantly lower than that in the control group,and the number of CD（19）~＋ B cells in germinal center was significantly decreased. Conclusion： There are significant differences in lymphocyte subsets distribution in tonsillar germinal center and interfollicular area between IgA nephropathy and chronic tonsillitis without kidney disease. The proliferation、differentiation and aggregation of lymphocytes in the tonsils of IgA nephropathy is different from normal people,mucosal immunity may be involved in the pathogensis of IgA nephropathy.