CAJ | 학술논문

目的探讨抗中性粒细胞胞质抗体(ANCA)对中性粒细胞表面FcγⅡ/Ⅲ(CD32/CD16)受体表达的影响及临床意义.方法提纯活动期ANCA相关性小血管炎(AASV)患者的ANCA IgG,分离健康人新鲜中性粒细胞,以ANCA刺激粒细胞1 h后,流式细胞仪检测CD32/CD16的表达.流式细胞仪检测18例系统性小血管炎患者CD32/CD16的表达,以35名健康人为对照.同时对18例患者临床表现及血管炎活动情况进行评分,与CD32/CDl6表达进行相关分析.结果 ANCA IgG与正常人IgG相比显著上调中性粒细胞表面CD16的表达(Mnx 67±23 vs 54±21,P<0.01),但对CD32的表达无影响(Mnx 21±8vs 16±8,P>0.05).系统性小血管炎患者CD16表达的平均荧光强度显著高于正常人(Mnx 62±12 vs 53±10.P<0.01),而CD32的表达与正常人差异无统计学意义.CD16表达与伯明翰小血管炎呈显著正相关(P<0.01).结论 ANCA相关性小血管炎患者高表达Fcγ受体,ANCA可以干预CD32/CD16受体的表达,调控FCγ受体表达可能是系统性小血管炎的发病机制之一,监测CD16的表达水平对于判断疾病活动具参考价值.
목적 탐토항중성립세포포질항체(ANCA)대중성립세포표면FcγⅡ/Ⅲ(CD32/CD16)수체표체적영향급림상의의.방법 제순활동기ANCA상관성소혈관염(AASV)환자적ANCA IgG,분리건강인신선중성립세포,이ANCA자격립세포1 h후,류식세포의검측CD32/CD16적표체.류식세포의검측18례계통성소혈관염환자CD32/CD16적표체,이35명건강인위대조.동시대18례환자림상표현급혈관염활동정황진행평분,여CD32/CDl6표체진행상관분석.결과 ANCA IgG여정상인IgG상비현저상조중성립세포표면CD16적표체(Mnx 67±23 vs 54±21,P<0.01),단대CD32적표체무영향(Mnx 21±8vs 16±8,P>0.05).계통성소혈관염환자CD16표체적평균형광강도현저고우정상인(Mnx 62±12 vs 53±10.P<0.01),이CD32적표체여정상인차이무통계학의의.CD16표체여백명한소혈관염정현저정상관(P<0.01).결론 ANCA상관성소혈관염환자고표체Fcγ수체,ANCA가이간예CD32/CD16수체적표체,조공FCγ수체표체가능시계통성소혈관염적발병궤제지일,감측CD16적표체수평대우판단질병활동구삼고개치.
Objective The interaction between anti-neutrophil cytoplasmic antibaties (ANCA) and receptors at the Fc portion of immunoglobulins (FeγR) is central in the pathogenisis of primary systemic small vasculitis. The aim of this study is to investigate the role and clinical value of ANCA on the expression of neutrophils FCγRⅡ/Ⅲ (CD32/CD16). Methods ANCA IgG was prepared from the sera of patients with active We-gener's granulomatosis (WG) and microscopic polyangiitis (MPA). Neutrophils were isolated from the blood of healthy volunteers. The expression of CD32/CD16 on neutrophils was assessed by flow cytometry after stimulated by ANCA for 1 hour. We compared the expression of CD32/CD16 between 18 primary systemic small vaseulitis (PSV) patients and 35 healthy volunteers. Furthermore, the correlation was also be analyzed between the expression of CD32/CD16 and Birmingham vasculitis activity score (BVAS). Results The expression of CD16 was significandy elevated by ANCA (Mnx 67±23 vs 54±21, P<0.01 ). The expression of CD16 was higher in patients than in healthy volunteers (Mnx 62±12 vs 53±10, P<0.01), which was in correlation with BVAS (r=0.728 86, P<0.01). But no such correlation was found for CD32 . Conclusion ANCA may play a role in the pathogenesis of PSV by modulating the expression of the FCγR. Monitoring the expression of CD16 on neutrophils is helpful for the evaluation of PSV activity. 86, P<0