CAJ | 학술논문

目的:通过研究趋化因子配体10(CXCL10)及其受体(CXCR3)的表达,探讨其参与子宫内膜异位症(EM)发病的免疫机制.方法:分别运用ELISA法及化学发光分析法检测EM患者未经手术治疗组(76例)、经手术治疗组(10例)及正常体检人员组(76例)血清标本中CXCL10及癌胚抗原CA125浓度;分离并体外活化EM患者组(10例)及正常体检人员组(10例)外周血单个核细胞(PBMC),ELISA法检测活化后PBMC培养上清液中CXCL10的分泌表达水平、流式细胞术检测活化PBMC的表面分化抗原3(CD3)及CXCR3表达、RT-PCR检测CXCR3基因亚群(CXCR3A及CXCR3B)的表达;对结果进行统计分析.结果:血清CXCL10水平,EM患者未经手术治疗组、经手术治疗组及正常体检人员组间比较均具有显著差异(P＜0.05);EM组与正常体检人员组比较:活化PBMC培养上清液中CXCL10的表达水平无显著差异(P>0.05)、CD3~+/CXCR3~+PBMC细胞数无显著差异(P>0.05)、EM组高转录表达CXCR3B亚群而正常对照组表达CXCR3A亚群.结论:EM患者的血清CXCL10缺陷表达可能是参与EM发病的免疫机制之一;EM患者PBMC对细胞活化信号具有有效的免疫反应性,但活化后的PBMC细胞表面高表达的是CXCR3B亚群、而非具有趋化效应的CXCR3A亚群,推测EM通过此种免疫逃逸机制而发病.
목적:통과연구추화인자배체10(CXCL10)급기수체(CXCR3)적표체,탐토기삼여자궁내막이위증(EM)발병적면역궤제.방법:분별운용ELISA법급화학발광분석법검측EM환자미경수술치료조(76례)、경수술치료조(10례)급정상체검인원조(76례)혈청표본중CXCL10급암배항원CA125농도;분리병체외활화EM환자조(10례)급정상체검인원조(10례)외주혈단개핵세포(PBMC),ELISA법검측활화후PBMC배양상청액중CXCL10적분비표체수평、류식세포술검측활화PBMC적표면분화항원3(CD3)급CXCR3표체、RT-PCR검측CXCR3기인아군(CXCR3A급CXCR3B)적표체;대결과진행통계분석.결과:혈청CXCL10수평,EM환자미경수술치료조、경수술치료조급정상체검인원조간비교균구유현저차이(P＜0.05);EM조여정상체검인원조비교:활화PBMC배양상청액중CXCL10적표체수평무현저차이(P>0.05)、CD3~+/CXCR3~+PBMC세포수무현저차이(P>0.05)、EM조고전록표체CXCR3B아군이정상대조조표체CXCR3A아군.결론:EM환자적혈청CXCL10결함표체가능시삼여EM발병적면역궤제지일;EM환자PBMC대세포활화신호구유유효적면역반응성,단활화후적PBMC세포표면고표체적시CXCR3B아군、이비구유추화효응적CXCR3A아군,추측EM통과차충면역도일궤제이발병.
AIM: To investigate the immunologic mechanism of CXC chemokine ligand 10(CXCL10) and its receptor CXC chemokine receptor 3 (CXCR3 ) involved in the process of endometriosis (EM). METHODS: Serum samples were collected from 3 groups; EM patients without operation (n = 76) , EM patients with operation (n = 10) and the normal control persons (n =76). CXCL10 and CA12S concentrations were detected by means of ELISA and chemilumino-metry. Cell surface antigens on the activated PBMC - CD3 and CXCR3, as well as CXCR3 subgene - CXCR3A and CX-CR3B were tested by flow cytometry (FC) and RT - PCR when PBMC was separated from women with EM ( n = 10) and without EM (n = 10), and then activated. RESULTS: Serum CXCL10 concentrations between three groups were signifi-canly different (P < 0.05). Compared to normal control group, although the supernatant CXCL10 concentration and CD3~+ /CXCR3~+ PBMC number in EM group has no significant difference (P >0.05) , highly expressed CXCR3B in EM group rather than CXCR3A was observed. CONCLUSION: CXCL10 in women with EM is low, indicating that it plays a vital role in the process of EM and immune system of the women with EM is defected and impaired. The immunoreactivity of PBMC from both EM patients and normal person is same to activated signal, but the productions are different: PBMC in EM group mainly express CXCR3B but PBMC in normal person mainly express CXCR3A after activation, which may be one of the immune mechanisms that EM escapes from immunological lethal effect of the infected host.