次级淋巴组织趋化因子及其受体对干燥综合征患者外周血淋巴细胞趋化性的影响

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目的:研究次级淋巴组织趋化因子(CCL21)及其受体(CCR7)对干燥综合征(SS)患者外周血淋巴细胞趋化性的影响,并探讨其在SS发病机制中的作用。方法:选择31例SS患者(其中原发性SS18例、继发性SS13例)及正常对照20例(均为健康体检者)。分离SS患者及正常对照的外周血淋巴细胞,采用transwell细胞跨膜试验检测CCL21/CCR7对外周血淋巴细胞迁移的影响。结果:在CCL21的作用下,原发性SS和继发性SS患者外周血淋巴细胞的趋化指数(CI)分别为2.92±0.12和2.80±0.28,均明显高于正常对照(CI=1.32±0.11,P<0.01);原发性SS和继发性SS患者之间淋巴细胞的CI无统计学差异(P>0.05)。经过抗CCR7单抗(mAb)处理后,原发性SS和继发性SS患者的CI分别为1.04±0.05和1.03±0.08,与未经抗CCR7mAb处理的SS患者相比较明显降低(P<0.01)。结论:CCR7是导致淋巴细胞迁移的重要因素之一。CCL21/CCR7的相互作用可介导SS患者外周血淋巴细胞的迁移,可能与SS患者的外分泌腺中大量淋巴细胞浸润导致腺体损害有重要关系。 Objective: To investigate the effects of secondary lymphoid chemokine (CCL21) and its receptor (CCR7) on the chemotaxis of peripheral blood lymphocytes in patients with Sjogren ’s syndrome (SS) and its role in the pathogenesis of SS. Methods: Thirty-one patients with SS (including 18 primary SS and 13 secondary SS) and 20 normal controls (all healthy subjects) were selected. Peripheral blood lymphocytes were isolated from peripheral blood mononuclear cells of SS patients and normal controls. The transwell assay was used to detect the effect of CCL21 / CCR7 on the migration of peripheral blood lymphocytes. Results: Under the action of CCL21, the chemotactic index (CI) of peripheral blood lymphocytes in patients with primary SS and secondary SS were 2.92 ± 0.12 and 2.80 ± 0.28, respectively, which were significantly higher than those of the normal controls (CI = 1.32 ± 0.11, P <0.01). There was no significant difference in CI of lymphocytes between patients with primary SS and those with secondary SS (P> 0.05). After treatment with anti-CCR7 mAb, the CIs in patients with primary SS and those with secondary SS were 1.04 ± 0.05 and 1.03 ± 0.08, respectively, which were significantly lower than those without CCR7 mAb (P <0.01) ). Conclusion: CCR7 is one of the important factors leading to lymphocyte migration. The interaction of CCL21 / CCR7 may mediate the migration of peripheral blood lymphocytes in patients with SS, which may be related to the large number of lymphocytes infiltration in the exocrine glands of SS patients leading to the damage of the gland.
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