Jaskłowska-Englisz M, Olszewski W L, Maksymowicz M, Ziółkowska A
Department for Surgical Research and Transplantology, Medical Research Centre, Polish Academy of Sciences, Warsaw, Poland.
Ann Transplant. 1998;3(1):28-33.
Organ allografts survive in hosts treated with immunosuppressive drugs. The question arises as to whether cells isolated from organ or tissue of an allogeneic donor and transplanted to a genetically disparate recipient can also benefit from the immunosuppressive regimen. We reported previously that the DST (donor specific transfusion) recipients accept heart allografts but reject hyperacutely i.v. infused lymphocytes from the same as DST donor. The present study was devoted to elucidation of the mechanism of these divergent processes. Syngeneic BN hearts and mesenteric lymph node lymphocytes were transplanted to LEW rats pretreated one week previously with donor specific blood transfusions. The allogeneic BN lymphocytes transplanted i.v. to LEW rats receiving one BN DST were rejected hyperacutely within 6 hrs, whereas BN heart grafts transplanted to the BN DST-treated LEW recipients survived 14 +/- 2 days. Adoptive transfer of LEW anti-BN DST sera to naive LEW rats caused destruction of the transplanted BN lymphocytes. The LEW BN DST recipients possessed IgG and IgM class alloantibodies binding to BN lymphocytes and heart endothelial cells. mAbs against MHC class I (OX18) and class II (OX6) antigens neither blocked binding of antibodies of DST-recipient sera to BN lymphocytes nor protected the preincubated BN lymphocytes against destruction after transplantation. Western blot analysis revealed that alloantibodies from DST-recipient sera bound strongly to BN lymphocyte membrane proteins of 60 kd m.w. but not to 45 kd and 30 kd MHC class I and II proteins. Taken together, DST has no protective effect on intravenously transplanted cells. In contrast, it accelerates the rejection. Alloantibodies present in DST-recipient sera "shield" antigens on the surface of organ allograft endothelial cells, thereby protecting them from recognition and cytotoxic effect. Simultaneously, these alloantibodies "opsonize" the intravenously transplanted lymphocytes and facilitate their halting in lymphoid organs and subsequent lysis. Antibodies other than those directed against MHC seem to mediate both these processes. The results of these studies provide also evidence that the effector mechanism of rejection may be different depending on location of the graft, in the lymphoid as in case of transplanted lymphocytes or in non-lymphoid tissues as heart grafts.
器官异体移植在接受免疫抑制药物治疗的宿主体内存活。问题在于,从异体供体的器官或组织中分离出来并移植到基因不同的受体中的细胞,是否也能从免疫抑制方案中获益。我们之前报道过,接受供体特异性输血(DST)的受体接受心脏异体移植,但会超急性排斥来自与DST供体相同个体的静脉输注淋巴细胞。本研究致力于阐明这些不同过程的机制。将同基因的BN心脏和肠系膜淋巴结淋巴细胞移植到一周前接受过供体特异性输血预处理的LEW大鼠体内。静脉注射到接受一次BN DST的LEW大鼠体内的异体BN淋巴细胞在6小时内被超急性排斥,而移植到接受BN DST治疗的LEW受体体内的BN心脏移植物存活了14±2天。将LEW抗BN DST血清过继转移到未接触过抗原的LEW大鼠体内,导致移植的BN淋巴细胞被破坏。接受BN DST的LEW受体拥有与BN淋巴细胞和心脏内皮细胞结合的IgG和IgM类同种异体抗体。针对MHC I类(OX18)和II类(OX6)抗原的单克隆抗体既不能阻断DST受体血清抗体与BN淋巴细胞的结合,也不能保护预先孵育的BN淋巴细胞在移植后免受破坏。蛋白质印迹分析显示,来自DST受体血清的同种异体抗体与分子量为60kd的BN淋巴细胞膜蛋白强烈结合,但不与45kd和30kd的MHC I类和II类蛋白结合。综上所述,DST对静脉移植的细胞没有保护作用。相反,它会加速排斥反应。DST受体血清中存在的同种异体抗体“屏蔽”了器官异体移植内皮细胞表面的抗原,从而保护它们免受识别和细胞毒性作用。同时,这些同种异体抗体“调理”静脉移植的淋巴细胞,并促进它们在淋巴器官中滞留并随后裂解。除了针对MHC的抗体之外的其他抗体似乎介导了这两个过程。这些研究结果还提供了证据,表明排斥反应的效应机制可能因移植物的位置而异,如移植淋巴细胞时在淋巴组织中,或如心脏移植物时在非淋巴组织中。