补体经典途径在泪腺良性淋巴上皮病变发生中的作用

目的：分析补体系统(CS)及其经典途径在泪腺良性淋巴上皮病变(LGBLEL)发病机制中的作用。

方法：采集LGBLEL患者和眼眶海绵状血管瘤(CH)患者的病变组织标本,使用蛋白质组学方法分析差异蛋白,而后采用逆转录-聚合酶链反应(RT-PCR)、免疫组织化学染色(IHC)和蛋白质印迹法(Western Blotting)验证CS信号通路中差异蛋白表达的变化,明确其在LGBLEL发病机制中的作用。

结果：蛋白质组学分析结果表明,相对于眼眶CH患者,LGBLEL患者病变泪腺组织中CS信号通路重要蛋白C3、C5、C9、C1q等表达均发生改变; RT-PCR检测结果显示,与眼眶CH患者相比,LGBLEL患者病变泪腺组织中C1qA、C5、C9 mRNA表达升高; 免疫组织化学染色结果显示,与眼眶CH患者相比,LGBLEL患者病变泪腺组织中C1qA、C3、C5、C9表达明显增多; Western Blotting检测结果显示,与眼眶CH患者相比,LGBLEL患者病变泪腺组织中C1qA、C3、C9蛋白表达水平明显升高。

结论：CS参与LGBLEL的发病机制,其经典途径可能是其发挥作用的途径之一。

Study on the role of classical complement pathway in the development of benign lymphoepithelial lesions of lacrimal gland

AIM: To analyze the role of complement system(CS)and its classical pathway in the pathogenesis of lacrimal gland benign lymphoepithelial lesions(LGBLEL).

METHODS: The tissues of patients with LGBLEL or orbital cavernous hemangioma(CH)were collected. Proteomics analysis was used for the identification of different proteins. Reverse transcription-polymerase chain reaction(RT-PCR), immunohistochemical staining(IHC)and Western Blotting were employed to verify the changes of the differential proteins in CS signal pathway, in order to identify its role in the pathogenesis of LGBLEL.

RESULTS: The results of proteomic analysis showed that the expression levels of proteins C3, C5, C9 and C1q in CS signal pathway in the lacrimal gland tissues of LGBLEL patients were all changed compared with those of orbital CH patients.The results of RT-PCR showed that the mRNA expression levels of C1qA, C5 and C9 in patients with LGBLEL were significantly higher than those patients with orbital CH. The results of IHC showed that the expression levels of C1qA, C3, C5 and C9 were significantly increased in patients with LGBLEL compared with those patients with orbital CH. The results of Western Blotting showed that the protein expression levels of C1qA, C3, and C9 were significantly increased in patients with LGBLEL compared with those patients with orbital CH.

CONCLUSION: The CS has been shown to participate in the pathogenesis of LGBLEL and its classical pathway may be one of the pathways which plays a role.