CAJ | 학술논문

目的探讨60 000相对分子质量SSA表位差异性表达与原发性干燥综合征(pSS)患者唾液腺(MSG)受累的相关性.方法利用噬菌体抗体展示技术筛选并可溶性表达针对3个SSA抗原表位(P1:480-494,P2:310-323和P3:230-241)特异性单克隆单链抗体(ScFv McAb),免疫组化法(IH)检测不同表位在pSS患者MSG的表达情况,并判断表达程度与MSG炎症是否存在相关性.结果 pSS MSG活检标本P1～P3表位的均有表达,以腺管、泌管上皮细胞胞质和胞膜着色为主.P1表位表达强度高于P2和P3表位(x2=12.94,P＜0.01),且仅P1表位表达强度与MSG的炎性浸润程度呈正相关关系(t=2.27,P＜0.05).结论 SSA抗原表位在MSG组织异位表达于上皮细胞的细胞膜,从而可能打破免疫耐受,诱导机体产生致病性抗体.P1表位在MSG膜高表达,而且仅P1与MSG炎症存在正相关关系,提示P1表位可能是引发pSS自身免疫应答的关键表位.
목적 탐토60 000상대분자질량SSA표위차이성표체여원발성간조종합정(pSS)환자타액선(MSG)수루적상관성.방법 이용서균체항체전시기술사선병가용성표체침대3개SSA항원표위(P1:480-494,P2:310-323화P3:230-241)특이성단극륭단련항체(ScFv McAb),면역조화법(IH)검측불동표위재pSS환자MSG적표체정황,병판단표체정도여MSG염증시부존재상관성.결과 pSS MSG활검표본P1～P3표위적균유표체,이선관、비관상피세포포질화포막착색위주.P1표위표체강도고우P2화P3표위(x2=12.94,P＜0.01),차부P1표위표체강도여MSG적염성침윤정도정정상관관계(t=2.27,P＜0.05).결론 SSA항원표위재MSG조직이위표체우상피세포적세포막,종이가능타파면역내수,유도궤체산생치병성항체.P1표위재MSG막고표체,이차부P1여MSG염증존재정상관관계,제시P1표위가능시인발pSS자신면역응답적관건표위.
Objective To investigate the correlation between the differential expression of 60 000SSA epitopes in minor salivary glands(MSG) from patients with primary Sj(o)gren's syndrome (pSS) and glandular inflammation. Methods The screening and soluble expression of single-chain fragment V monoclonal antibodies (Scfv McAb) against SSA antigen epitopes ( P1: 480-494, P2: 310-323 and P3: 230-241 )were performed by phagmid antibody expression system. The expression of epitopes was detected by immunohistochemical assay (IH) in minor salivary glands from these patients. The correlation between epitopes expression and glandular inflammation was analyzed quantitatively. Results Immunohistochemical assay of MSG with McAb against P1-P3 epitopes showed that the epithelial cells of glandular tubes and striated duct were stained in membrane and cytoplasm. The expression of P1 epitope was higher than the other two in grading score (x2 = 12. 94, P ＜ 0. 01 ). And a positive correlation was found between the extent of glandular infiltration and the grade of P1 epitope expression(t =2. 27, P ＜0. 05) but not with P2 or P3 epitope. Conclusion Aberrant redistribution of intracellular SSA antigen epitopes onto the cell membrane of involved cells may break the immune tolerance and thus induce the production of pathogenic autoantibodies involved in triggering and maintaining the tissue-specific autoimmune response in pSS MSG. A significantly high membranous expression of P1 and a positive correlation between P1 and the inflammation of MSG suggest that P1 may be the dominant determinant of the antigen-driven immune response in pSS.