Prevention of hyperacute xenograft rejection by polyclonal antibodies

通过针对供者淋巴细胞和红细胞的多克隆抗体来预防超急性异种移植排斥反应。据报道，高剂量的免疫球蛋白(IVIG)静脉注射可延缓异种移植物超急性排斥反应的发生。为探讨静脉注射丙种球蛋白(IVIG)预防豚鼠心脏移植HAR的可能性，在移植前即刻用豚鼠淋巴细胞和红细胞免疫兔制备了特异性多克隆抗体(抗GP-Pab)，Lewis大鼠静脉注射20%人血清白蛋白1ml或1.5-30 mg/kg。血管化异种心脏移植物的收缩时间从平均12.2min延长到7小时以上，这与注射抗体的剂量密切相关(r=0.958)。免疫病理检查发现，排斥移植物中C3和纤维蛋白原弥漫性沉积，少量大鼠免疫球蛋白M血管沉积。在抗体处理的功能移植物中，移植后早期即可观察到兔的免疫球蛋白沿内皮细胞沉积，而免疫球蛋白C_3、纤维蛋白原和大鼠的免疫球蛋白M沉积较少。综上所述，我们的数据提示兔抗GP-Pab。在高剂量下，阻止天然抗体与移植物内皮的结合，调节补体的激活。

Prevention of hyperacute xenograft rejection by polyclonal antibodies against donor luymphocytes and red cells.T.Murakami, S.Hujita, Y.Hayasaka, M.Shinkai, Y.Funakoshi, T.Kawai, S.Fuchinoue, S.Teraoka, T.Agishi, and K.Ota.Dept.of Surgery, Kidney Center, Tokyo Womens Medical College, Tokyo, Japan.Intravenous administration of immunoglobulin (IVIG) at a high dosage has been reported to delay an initiation of hyperacute rejection (HAR) of the discordant xeno-grafts. In order to investigate possibility of preventing HAR of guinea pig hearts grafted to Lewis rats by IVIG,specific polyclonal antibodies were produced by immunizing rabbits against guinea pig lymphocytes and red cells (anti-GP-pAb)Immediately before transplantation, the Lewis rats intravenously received either 1 ml of 20% human albumin as a control or 1.5-30mg/kg of the antibodies. Contraction time of the vascualized cardiac xenografts was extended from a mean of 12.2 minutes to longer than 7 hours intimately depending upon the doses of the antibodies administered (r=0.958). Immunopathological studing showed diffuse deposition of C3 and fibrinogen with a small amount of vascular deposits of rat IgM in the rejected grafts. In the functioning grafts treated with the antibodies, rabbit IgG deposition along endothelium was observed early after transplantation and becam more extensive with toime, while deposits of C3, fibrinogen and rat IgM were minimal. In conclusion, our data suggest that the rabbit antiGP-pAb. at a high dosage prevent the binding of the natural antibodies to the graft endothelium and modulate the complement activation.