Lück R, Klempnauer J, Steiniger B
Klinik für Abdominal- und Transplantationschirurgie, Medizinische Hochschule Hannover, Germany.
Transpl Int. 1994 Aug;7(5):344-8. doi: 10.1007/BF00336710.
The genetic requirements for the development of graft-versus-host (GVH) disease have been investigated in a model of semiallogenic, heterotopic small-bowel transplantation in the rat. Following semiallogenic MHC-incompatible small-bowel transplantation, all graft recipients showed characteristic signs of GVH disease and died within 14 days. On autopsy the transplanted bowel was normal, while the recipient's bowel was dilated and distended with gas. Histology showed a generalized cell infiltration of the connective tissue with macrophages and lymphocytes. After semiallogenic, RT1.A-incompatible, small-bowel transplantation, the graft recipients developed mild and temporary symptoms of GVH disease between days 25 and 40. Only two of the six animals died, while the remaining animals survived the observation period. Small-bowel transplantation across an isolated RT1.C barrier was unable to induce GVH reaction. These results indicate that the development of GVH disease after small-bowel transplantation is controlled genetically by the MHC. Class II MHC incompatibility is necessary for the induction of an acute and lethal GVH reaction.
在大鼠半同种异体异位小肠移植模型中，已对移植物抗宿主（GVH）病发展的遗传要求进行了研究。半同种异体MHC不相容的小肠移植后，所有移植物受体均表现出GVH病的特征性体征，并在14天内死亡。尸检时，移植的肠管正常，而受体的肠管扩张并充满气体。组织学显示结缔组织有巨噬细胞和淋巴细胞的全身性细胞浸润。半同种异体、RT1.A不相容的小肠移植后，移植物受体在第25天至40天之间出现了轻度和暂时性的GVH病症状。六只动物中只有两只死亡，其余动物在观察期内存活。跨越孤立的RT1.C屏障进行小肠移植无法诱导GVH反应。这些结果表明，小肠移植后GVH病的发展受MHC基因控制。II类MHC不相容是诱导急性致死性GVH反应所必需的。
