Salam A, Vandeputte M, Waer M
Transplantation Laboratory, Rega Institute, Leuven, Belgium.
Transpl Int. 1994;7 Suppl 1:S457-61. doi: 10.1111/j.1432-2277.1994.tb01418.x.
The evolution of Vbeta6-expressing C3H (H2k, Thy 1.2, Mls a-) lymphocytes was investigated in C3H recipients mice pretreated with total body irradiation (TBI) or total lymphoid irradiation (TLI) and infusion of AKR (H2k, Thy 1.1, Mls a+) cells. After TBI (9.5 Gy) all Vbeta6+ Thy 1.2 (C3H) cells, which are capable of reacting against the Mls a antigen that like expressed by AKR mice, were deleted in the thymus and the periphery in stable bone marrow (BM) chimeras obtained by infusion of 5 x 10(6) T-cell-depleted (TCD) AKR BM cells. When, in the opposite combination, 30 x 10(6) C3H spleen cells were infused into TBI-treated AKR cells, all animals developed graft-versus-host disease (GVHD) with no clonal deletion and in contrast, showed an increase in Vbeta6+ C3H cells. After injection of 30 x 10(6) AKR BM cells into TLI-treated C3H mice no C3H cells were detected in the thymus and only a small percentage in the periphery. Within these C3H cells Vbeta6+ cells were only partially deleted and anergized as they did not respond in vitro after stimulation with Mls a+ AKR cells or anti-Vbeta6 mAb. Cells suppressing anti-Mls a-reacting C3H cells were not found. After injection of 15 x 10(6) AKR cells more C3H cells were found in the thymus, but only a minority of Vbeta6+ cells persisted in the periphery of these animals. In conclusion in TBI-prepared chimeras only clonal deletion occurred, whereas in TLI-prepared chimeras both clonal deletion and anergy occurred in maintaining tolerance.
在接受全身照射（TBI）或全淋巴照射（TLI）并输注AKR（H2k，Thy 1.1，Mls a +）细胞预处理的C3H受体小鼠中，研究了表达Vbeta6的C3H（H2k，Thy 1.2，Mls a -）淋巴细胞的演变。在TBI（9.5 Gy）后，所有能够对AKR小鼠表达的Mls a抗原产生反应的Vbeta6 + Thy 1.2（C3H）细胞，在通过输注5 x 10（6）个T细胞耗竭（TCD）AKR骨髓细胞获得的稳定骨髓（BM）嵌合体的胸腺和外周中被删除。相反，当将30 x 10（6）个C3H脾细胞输注到经TBI处理的AKR细胞中时，所有动物都发生了移植物抗宿主病（GVHD），没有克隆缺失，相反，Vbeta6 + C3H细胞增加。将30 x 10（6）个AKR骨髓细胞注射到经TLI处理的C3H小鼠中后，在胸腺中未检测到C3H细胞，在外周中仅检测到一小部分。在这些C3H细胞中，Vbeta6 +细胞仅被部分删除并失能，因为它们在用Mls a + AKR细胞或抗Vbeta6单克隆抗体刺激后在体外没有反应。未发现抑制抗Mls a反应的C3H细胞的细胞。注射15 x 10（6）个AKR细胞后，在胸腺中发现了更多的C3H细胞，但在这些动物的外周中仅少数Vbeta6 +细胞持续存在。总之，在TBI制备的嵌合体中仅发生克隆缺失，而在TLI制备的嵌合体中，在维持耐受性时发生克隆缺失和失能。
