CAJ | 학술논문

目的观察人软骨糖蛋白-39( HCgp39)对胶原诱导型关节炎(CIA)大鼠淋巴细胞激活的影响,探讨其在类风湿关节炎(RA)发病中的作用.方法建立CIA大鼠模型,分别在建模1、2、3、4、5、6、7、8周后,分离、培养大鼠脾淋巴细胞,CCK-8法检测HCgp39对淋巴细胞增殖的影响,ELISA法检测血浆中抗HCgp39抗体及COMP的分泌水平,分析指标之间相关性.结果建模2周后,HCgp39抗原特异性T细胞与对照组比较出现明显增殖反应(P均＜0.01),与建模时间、抗HCgp39抗体水平显著正相关,与血管翳和滑膜炎症评分显著负相关.各组抗HCgp39抗体水平和COMP水平较对照组显著增高(P均＜0.01),且抗HCgp39抗体水平与建模时间及COMP呈显著正相关.结论 HCgp39可刺激CIA大鼠脾淋巴细胞的体外异常增殖,初步提示HCgp39抗原短肽在CIA早期及后续的发病过程中可能起着一定作用.
목적 관찰인연골당단백-39( HCgp39)대효원유도형관절염(CIA)대서림파세포격활적영향,탐토기재류풍습관절염(RA)발병중적작용.방법 건립CIA대서모형,분별재건모1、2、3、4、5、6、7、8주후,분리、배양대서비림파세포,CCK-8법검측HCgp39대림파세포증식적영향,ELISA법검측혈장중항HCgp39항체급COMP적분비수평,분석지표지간상관성.결과 건모2주후,HCgp39항원특이성T세포여대조조비교출현명현증식반응(P균＜0.01),여건모시간、항HCgp39항체수평현저정상관,여혈관예화활막염증평분현저부상관.각조항HCgp39항체수평화COMP수평교대조조현저증고(P균＜0.01),차항HCgp39항체수평여건모시간급COMP정현저정상관.결론 HCgp39가자격CIA대서비림파세포적체외이상증식,초보제시HCgp39항원단태재CIA조기급후속적발병과정중가능기착일정작용.
Objective To examine the proliferative effect of synthetic cyclic human cartilage glycoprotein-39 (HCgp39) on T cell of collagen-induced arthritis (CIA) rat,and to explore the role of HCgp39 in rheumatoid arthritis (RA).Methods We established the rat model of the collagen-induced arthritis (CIA).The T lymphocytes were isolated and incubated with HCgp39.Proliferation of T cells was determined by cell counting kit-8.Results Two weeks after the first immunization,T cell response to HCgp39 was more significant in CIA groups than in controls( P＜0.01 ),and the response was associated with disease course ( r =0.732,P＜0.01 ) and anti- HCgp39 antibody ( r =0.460,P＜0.01 ).A strong correlation between T cell proliferation and pannus ( r =-0.516,P＜0.01 ),synovium score ( r =-0.346,P＜0.01 ) was also observed.Besides,the levels of anti- HCgp39 antibody and comp in each CIA group were significantly higher than in controls( P＜0.01 ),and the anti- HCgp39 antibody strongly correlated with disease course( r=0.346,P＜0.01 ) and comp( r =0.235,P＜0.01 ).Conclusion The proliferative response of T cell to HCgp39 was found in the early stage of CIA rat,and the HCgp39 peptide antibody was detected in serum,suggesting that the HCgp39 antigen plays an important role in the pathogenesis of early RA.