Conti F, Grude P, Calmus Y, Scoazec J Y
Laboratoire de Biologie Cellulaire, Hôpital Cochin, INSERM U327, Faculté de Médecine Xavier Bichat, Paris, France.
J Hepatol. 1997 Nov;27(5):881-9. doi: 10.1016/s0168-8278(97)80326-1.
BACKGROUND/AIMS: In order to test the possible role of activated complement in human liver allograft rejection, we evaluated the expression of the membrane attack complex of complement, its soluble inhibitors clusterin and vitronectin and its membrane inhibitor protectin during the evolution of liver transplants.
An indirect immunoperoxidase technique was applied to biopsy specimens obtained from liver allografts in 16 patients without complications, nine with acute rejection, four with chronic rejection and five with biliary complications.
Two types of membrane attack complex deposition were observed: (a) extracellular deposits in portal tracts and perisinusoidal matrix, associated with clusterin and vitronectin, similar to those found in the normal liver; and (b) intra-portal vascular deposits, devoid of clusterin and vitronectin. Vascular membrane attack complex deposition was detected in four clinically stable patients, three patients with chronic rejection and two patients with biliary complications. In clinically stable patients, vascular membrane attack complex deposition was restricted to large portal vessels and was detected in a minority of portal tracts. In patients with chronic rejection or biliary complications, vascular membrane attack complex deposition was detected along both large and small portal vessels and was present in the majority of portal tracts. Protectin induction on hepatocytes was detected in 33 cases.
Our results suggest that membrane attack complex deposition is unlikely to play a major role in the pathogenesis of acute liver allograft rejection but may contribute to the vascular and biliary lesions observed in chronic rejection.
背景/目的：为了检验活化补体在人类肝脏同种异体移植排斥反应中可能发挥的作用，我们评估了补体膜攻击复合物、其可溶性抑制剂簇集素和玻连蛋白以及其膜抑制剂保护素在肝脏移植过程中的表达情况。
采用间接免疫过氧化物酶技术，对16例无并发症、9例急性排斥反应、4例慢性排斥反应和5例胆道并发症的肝脏同种异体移植患者的活检标本进行检测。
观察到两种类型的膜攻击复合物沉积：(a) 门管区和窦周基质中的细胞外沉积物，与簇集素和玻连蛋白相关，类似于正常肝脏中的沉积物；(b) 门脉内血管沉积物，缺乏簇集素和玻连蛋白。在4例临床稳定的患者、3例慢性排斥反应患者和2例胆道并发症患者中检测到血管膜攻击复合物沉积。在临床稳定的患者中，血管膜攻击复合物沉积仅限于大型门脉血管，且仅在少数门管区检测到。在慢性排斥反应或胆道并发症患者中，沿大型和小型门脉血管均检测到血管膜攻击复合物沉积，且存在于大多数门管区。33例患者检测到肝细胞上有保护素诱导表达。
我们的结果表明，膜攻击复合物沉积不太可能在急性肝脏同种异体移植排斥反应的发病机制中起主要作用，但可能与慢性排斥反应中观察到的血管和胆道病变有关。
