In der letzten Zeit meint man, es handele sich um immunologisches Enhancement, wenn ein Empfänger verlängert überlebt, sei es durch Immunsuppression, sei es durch Alloantiserumbehandlung oder durch Vorbehandlung mit Spenderspezifischem Antigen. Bei „major“ histocompatiblen Kombinationen mit „minor“ Histoincompatibilität ist man unterschiedlicher Meinung. Hildemann und White (1) meinen, daß die Empfänger bei der schwach histoincompatiblen Kombination durch immunologisches Enhancement verlängert überlebten. Mahabir und Guttman (2) verneinen dies. Daher haben wir in dieser Arbeit versucht zu klären, durch welchen Mechanismus Allotrans- plantatempfänger (LEW-Ratten) nach Fisher (Fi)- und (Fi x LEW)F1- Nierenverpflanzung verlängert überlebten.

To study the immunological status of indefinitely surviving recipients of histocompatible (minor histoincompatible) allografts we transplanted Fi or (Fi x LEW)F1-kidneys to LEW-rats. At the same time bilateral nephrectomy was performed. To examine the cellular immune response we carried out local GvHR, microcytotoxicity assay and allorosette-formation test with recipient cells. We also studied lymphocytotoxins in the serum of recipients. To detect a blocking serum factor we used allorosette-formation inhibition test and microcytotoxicity assay. A blocking serum factor could not be found. In spite of stimulation with donor specific skin graft the cellular immune response of prolonged surviving recipients was inhibited. Our results suggest that prolonged survival of minor histoincompatible renal allograft recipients was caused by suppression of cellular immune response.

Um den immunologischen Status der schwach histoinkompatiblen Rattennierenempfänger zu prüfen, verpflanzten wir bei LEW-Ratten FiS- bzw. FLF1-Nieren. Die FiS-Nierenempfänger starben fast alle innerhalb von 55 Tagen; nur 4 von 24 Tieren überlebten länger als 4 Monate. Zwei Drittel der FLF1-Nierenempfänger überlebten jedoch länger als 4 Monate; das restliche Drittel nur bis zu 64 Tagen.

Thirty-nine (LEW x BN)F1 kidneys were transplanted to LEW rats. Twenty-four untreated recipients survived for a mean time of 16.1 +/- 1.7 days (group 1). Fifteen recipients received 4 ml of antilymphocytic serum per rat (group 3). In the last group 10 recipients survived for more than 4 months. The spleen cells of these permanently surviving 10 rats were obtained by splenectomy and used in a graft-versus-host assay, and this assay showed that the reactivity of these cells was normal. Following splenectomy the animals were given an (LEW x BN)F1 skin allograft, followed 18 days by a second. After another 18 days (LEW x Buf)F1 "third party" skin allografts were transplanted to the same animals. Animals of group 2 rejected their first grafts with a mean survival time of 12.2 +/- 1.2 days, whereas the second grafts were rejected normally as were the third party grafts. Attempts were made to detect lymphocytotoxic antibodies and haemagglutinins before and after the transplantation of skin grafts and none could be found up to day 53. The sera of group 2 inhibited allorosette formation by 38%. This serum-blocking factor was donor specific. It is probable that the survival of the kidney transplants following antilymphocytic serum treatment was brought about by the development of blocking antibodies.

Summary To study the immunological status of recipients of major compatible and minor incompatible kidney allografts, we transplanted FiS and FLF1 kidneys into LEW rats. Most of the FiS kidneys were rejected within 55 days. Of 24 recipients, only 4 survived longer than 4 months. However, two-thirds of the FLF1 recipients survived longer than 4 months. The other third died within 64 days.