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目的:以扁桃体隐窝内甲型链球菌(HS)灭活菌株刺激IgA肾病(IgAN)患者和非肾炎患者扁桃体淋巴细胞,观察未刺激及刺激后CD4+CD25+细胞和分泌J链IgA细胞数量,探讨IgAN的发病机制。方法:(1)收集37例IgAN患者及37例非肾炎慢性扁桃体炎患者手术摘除的扁桃体;(2)分离鉴定两组患者扁桃体隐窝内细菌及分离培养扁桃体淋巴细胞;(3)以分离最多的灭活菌株HS体外刺激扁桃体淋巴细胞72h;(4)以流式细胞仪检测扁桃体淋巴细胞CD4+CD25+细胞数,以原位杂交技术检测J链mRNA表达,以免疫荧光及荧光原位杂交技术同步分析分泌J链IgA细胞。结果:(1)两组患者均有甲型链球菌,且甲型链球菌在分离的细菌中是最多的。两组患者的细菌谱和细菌量无统计学差异。(2)未刺激、非肾炎患者HS(HS-controls)、IgAN患者HS(HS-IgAN)刺激后CD4+CD25+细胞数[(0.98±0.204)% vs (3.58±0.554)%,P<0.05,(1.37±0.214)% vs (5.78±0.562)%,P<0.05,and(1.43±0.202)% vs (6.05±0.521)%,P<0.05],IgAN组与非肾炎组比较,前者均显著低于后者。HS对IgAN组CD4+CD25+细胞的刺激指数(stimulation index,SI)显著低于非肾炎组(P均<0.05)。(3)未刺激、HS-controls、HS-IgAN刺激后J链mRNA阳性IgA细胞[(11.9±3.1)% vs (6.5±1.5)%,P<0.05,(33.5±5.7)% vs (13.9±1.2)%,P<0.05,and(35.1±6.2)% vs (13.9±1.2)%,P<0.01],IgAN组与非肾炎组比较,前者均显著高于后者。HS对IgAN组J链mRNA阳性IgA细胞的SI显著高于非肾炎组(P均<0.01)。(4)HS对CD4+CD25+细胞的SI与对分泌J链IgA细胞的SI呈显著性负相关(P均<0.01)。结论:IgAN患者扁桃体CD4+CD25+细胞减少和分泌J链IgA细胞增多可能与IgAN的发病机制有关。
OBJECTIVE: To stimulate tonsillar lymphocytes of patients with IgA nephropathy (IgAN) and non-nephritis with inactivated strains of Streptococcus mutans (HS) in tonsil crypts and to observe the numbers of CD4 + CD25 + cells and J-chain IgA secreting cells after stimulation and stimulation, To investigate the pathogenesis of IgAN. Methods: (1) Surgical removal of tonsil from 37 patients with IgAN and 37 patients with chronic non-nephritis chronic tonsillitis; (2) Isolation and identification of tonsil lymphocytes in two groups of patients; (3) (4) Flow cytometry was used to detect the number of CD4 + CD25 + cells in tonsil lymphocytes. The expression of J-chain mRNA was detected by in situ hybridization. The immunofluorescence and fluorescence in situ hybridization Simultaneous analysis of secreted J chain IgA cells. Results: (1) Streptococcus mutans were found in both groups, and Streptococcus mutans were the most abundant in isolated bacteria. There was no significant difference in bacterial spectrum and bacteria between the two groups. (2) The number of CD4 + CD25 + cells in unstimulated and non-nephritic HS (HS-controls) and IgAN patients after HS-IgAN stimulation was significantly higher than that in HS- (1.37 ± 0.214)% vs (5.78 ± 0.562)%, P <0.05, and (1.43 ± 0.202)% vs (6.05 ± 0.521)%, P <0.05). The former was significantly lower in IgAN group than in non-nephritis group In the latter. The stimulation index (SI) of HS group on CD4 + CD25 + cells in IgAN group was significantly lower than that in non-nephritis group (all P <0.05). (3) The expression of J chain mRNA positive IgA cells after stimulation with HS-controls and HS-IgAN was (11.9 ± 3.1)% vs (6.5 ± 1.5)%, P <0.05, (33.5 ± 5.7)% vs 1.2%, P <0.05, and (35.1 ± 6.2)% vs (13.9 ± 1.2)%, P <0.01]. The former was significantly higher than the latter in IgAN group and non-nephritis group. The SI of J chain mRNA positive IgA cells in IgAN group was significantly higher than that in non - nephritic group (all P <0.01). (4) The SI of CD4 + CD25 + cells was significantly and negatively correlated with the SI of secreting J chain IgA cells (all P <0.01). Conclusion: The decrease of tonsillar CD4 + CD25 + cells and the increase of J chain IgA cells in IgAN patients may be related to the pathogenesis of IgAN.