Stuart F P, Scollard D M, McKearn T J, Fitch F W
Transplantation. 1976 Nov;22(5):455-66. doi: 10.1097/00007890-197611000-00008.
Enhancement of LBN F1 renal allograft survival in Lewis (L) rats is achieved by injecting the recipient i.v. with donor antigen (LBN F1 spleen cells) 1 day before transplantation and antidonor antibody (L anti-BN alloantiserum) at the time of transplantation. Treatment with this combination of antigen and antibody also induces the recipient to make L anti-(L anti-BN) anti-idiotypic antibody that reaches peak titers within 10 days. The degree of graft enhancement achieved was increased greatly by delaying transplantation until the peak of the anti-idiotypic antibody response 10 days after treatment with antigen and antibody. Two in vitro assays for cellular immunity (51Cr release and microcytotoxicity) failed to demonstrate antidonor activity in spleen cells from recipients for which transplantation had been delayed 10 days. The close correlation of enhancement, absence of cellular immunity in vitro, and the kinetics of the anti-idiotypic antibody response suggest that anti-idiotypic antibody may prevent either sensitization and generation of effector T lymphocytes or the destructive potential of sensitized cells.
通过在移植前1天经静脉给受体注射供体抗原(LBN F1脾细胞)并在移植时注射抗供体抗体(L抗BN同种异体抗血清),可提高Lewis(L)大鼠中LBN F1肾移植的存活率。用这种抗原和抗体组合进行治疗还可诱导受体产生L抗(L抗BN)抗独特型抗体,该抗体在10天内达到峰值滴度。通过将移植推迟至抗原和抗体治疗后10天抗独特型抗体反应的峰值,所实现的移植增强程度大大提高。两种细胞免疫的体外检测方法(51Cr释放和微量细胞毒性)未能在移植已推迟10天的受体脾细胞中证明抗供体活性。移植增强、体外细胞免疫缺失和抗独特型抗体反应动力学之间的密切相关性表明,抗独特型抗体可能会阻止致敏和效应T淋巴细胞的产生,或阻止致敏细胞的破坏潜能。