Anderson N D, Wyllie R G, Shaker I J
Johns Hopkins Med J. 1977 Sep;141(3):135-47.
Unmodified rejection of rat renal allografts was characterized by the early onset and rapid progression of endothelial damage in venules and capillaries which culminated in ischemic cortical necrosis. This pattern of endothelial injury correlated with lymphocyte accumulation in vascular lumens and could not be duplicated by renal perfusion with alloantibodies or prevented by C'3 depletion. In contrast, endothelial integrity and normal graft function were maintained over study intervals extending to 200 days when Brown Norway (BN) rat kidneys were transplanted into Lewis (Le) rat kidney recipients subjected to neonatal thymectomy or lymph drainage. Vascular lesions occurred when syngeneic thoracic duct lymphocytes were transfused into these recipients, but irreversible endothelial injury could be prevented by simultaneous injections of immune plasma. These findings indicate that the destruction of donor endothelium is mediated by thymus-dependent immune mechanisms which can be altered by thoracic duct drainage to promote indefinite survival of renal allografts across major histocompatibility loci.
大鼠肾移植的未修饰排斥反应的特征是小静脉和毛细血管内皮损伤早发且进展迅速，最终导致缺血性皮质坏死。这种内皮损伤模式与血管腔内淋巴细胞积聚相关，且不能通过用同种抗体进行肾脏灌注来复制，也不能通过C'3耗竭来预防。相比之下，当将棕色挪威（BN）大鼠肾脏移植到接受新生儿胸腺切除术或淋巴引流的刘易斯（Le）大鼠肾脏受体中时，在长达200天的研究期间内皮完整性和移植肾功能得以维持。当将同基因胸导管淋巴细胞输注到这些受体中时会出现血管病变，但通过同时注射免疫血浆可预防不可逆的内皮损伤。这些发现表明，供体内皮的破坏是由胸腺依赖性免疫机制介导的，胸腺依赖性免疫机制可通过胸导管引流改变，从而促进跨越主要组织相容性位点的肾移植长期存活。
