CAJ | 학술논문

目的：检测肾移植受者术前血清内多反应性 IgG 抗体亚型与凋亡细胞的反应性及与补体激活途径的关系，初步探讨此类抗体导致移植肾排异反应及影响移植肾存活的机制。方法选取50例肾移植患者术前血清学标本，应用流式细胞技术检测血清内 IgG 抗体亚型（IgG1-IgG4）对凋亡细胞的反应性，并检测此类抗体与凋亡细胞反应后，能否激活补体途径，导致 C4d 沉积于靶细胞表面，并分析 IgG 亚型对凋亡细胞反应强度与 C4d 在靶细胞表面沉积强度的相关性。结果肾移植患者血清内 IgG 抗体对凋亡细胞的反应性主要由 IgG1及 IgG3亚型介导，而极少患者的血清由 IgG2或 IgG4介导对凋亡细胞的反应，IgG1及 IgG3亚型对凋亡细胞的反应性与 C4d 在靶细胞表面沉积强度呈显著相关性（P ＜0．001，P ＝0．005）。结论本研究初步揭示肾移植患者血清内多反应性 IgG 抗体通过 IgG1及IgG3亚型介导对凋亡细胞的反应性，并可能通过激活补体途径造成移植肾损伤。
목적：검측신이식수자술전혈청내다반응성 IgG 항체아형여조망세포적반응성급여보체격활도경적관계，초보탐토차류항체도치이식신배이반응급영향이식신존활적궤제。방법선취50례신이식환자술전혈청학표본，응용류식세포기술검측혈청내 IgG 항체아형（IgG1-IgG4）대조망세포적반응성，병검측차류항체여조망세포반응후，능부격활보체도경，도치 C4d 침적우파세포표면，병분석 IgG 아형대조망세포반응강도여 C4d 재파세포표면침적강도적상관성。결과신이식환자혈청내 IgG 항체대조망세포적반응성주요유 IgG1급 IgG3아형개도，이겁소환자적혈청유 IgG2혹 IgG4개도대조망세포적반응，IgG1급 IgG3아형대조망세포적반응성여 C4d 재파세포표면침적강도정현저상관성（P ＜0．001，P ＝0．005）。결론본연구초보게시신이식환자혈청내다반응성 IgG 항체통과 IgG1급IgG3아형개도대조망세포적반응성，병가능통과격활보체도경조성이식신손상。
Objective To investigate the association between reactivity of IgG subclass in kidney transplant recipi-ents to apoptotic cells and complement activation and explore the mechanism of effect of polyreactiveIgG on kidney al-lograft rejection and graft loss.Methods Pre-transplant serum samples were selected form 50 kidney transplant recipi-ents.Reactivity of IgG subclass to apoptotic cells was detected using flow cytometry.We also observed whether polyre-active IgG could activate complement pathway,leading C4d deposition on target cells after binding to apoptotic cells. The association between reactivity of IgG subclass to apoptotic cells and C4d deposition on target cells was analyzed. Results Our studies showed that IgG reactivity to apoptotic cells was almost exclusively mediated by IgG1 and IgG3 subclasses.Few samples showed IgG2 or IgG4reactivity to apoptotic cells.Moreover,we observed a strong association between IgG1 and IgG3 reactivity to apoptotic cells and C4d deposition on target cells (P <0.001,P =0.005).Conclu-sion Our studies preliminarily revealed that reactivity of polyreactive IgG in kidney transplant recipients to apoptotic cells was mediated by IgG1 and IgG3 subclasses,they lead to kidney allograft injury probably through activation of complement pathway.