Analysis of Thl/Th2 imbalance of systemic lupus erythematosus

目的：趋化因子受体CCR5和CCR4在Th1和Th2细胞上的表达存在差异。为了确定趋化因子受体在狼疮肾炎患者中是否存在差异表达，我们检测了狼疮肾炎患者外周血淋巴细胞和浸润到肾组织中的单个核细胞上CCR4和CCR5的表达。采用流式细胞术检测系统性红斑狼疮（SLE）患者外周血CD4^+ CD45RO^+细胞表面CCR4和CCR5的表达，并进行比较。健康的对照。同时分析CCR4^+或CCR5^+细胞绝对数与临床参数的相关性。采用免疫组化方法检测SLE患者肾组织单核细胞浸润中CCR4、CCR5和CD4的表达。CCR4^+的绝对数量，而不是CCR5^+，SLE患者外周血T淋巴细胞显著低于健康对照组，且与血清补体第三成分（C3）水平呈正相关。和50%溶血单位补体（CH 50）。狼疮性肾炎患者肾组织中浸润的CD4^+ T淋巴细胞大多表达CCR4，而不表达CCR5。结论：狼疮性肾炎患者外周血中CCR4^+ T淋巴细胞作为Th2细胞优先向肾组织迁移。CCR4^+ T淋巴细胞的分布异常可能参与了狼疮性肾炎的发病过程

Objective; Some chemokine receptors such as CCR5 and CCR4 are differentially expressed on Th1 and Th2 cells. To determine whether differential expression of the chemokine receptors was observed in patients with lupus nephritis, we examined the expression of CCR4 and CCR5 on peripheral blood lymphocytes and mononuclear cells infiltrated into renal tissue of patients with lupus nephritisMethods; The expression of CCR4 and CCR5 on CD4^+ CD45RO^+ cells was analyzed by flow cytometry and compared between patients with systemic lupus erythematosus (SLE) and healthy controls. Correlation between the absolute number of CCR4^+ or CCR5^+ cells and clinical parameters was also analyzed. Mononuclear infiltrates in the renal tissue of SLE patients were analyzed for the expression of CCR4, CCR5, and CD4 by immunohistochemical staining.Results; The absolute number of CCR4^+, but not CCR5^+ , T lymphocytes in the peripheral blood (PB) was significantly decreased in the patients with SLE compared to that in healthy controls and positively correlated with the serum levels of 3rd component of complement (C3) and 50% hemolytic unit of complement (CH50). Most of the CD4^+ T lymphocytes that infiltrated into the renal tissue of the patients with lupus nephritis expressed CCR4 but not CCR5Conclusion; These results suggested that CCR4^+ T lymphocytes in PB, which represent Th2 cells, preferentially migrated into the renal tissue of the patients with lupus nephritis. The maldistribution of CCR4^+ T lymphocytes might be involved in the pathogenesis of lupus nephritis