Parkman R, Rappeport J, Rosen F
J Invest Dermatol. 1980 May;74(5):276-9. doi: 10.1111/1523-1747.ep12543412.
Human graft versus host disease is composed of 2 distinct clinical entities, acute graft versus host disease and chronic graft versus host disease, which have different pathogenesis. Acute graft versus host disease is produced by the attack of donor immunocompetent T or null lymphocytes against recipient histocompatibility antigens. The null lymphocytes may attack antigens shared by the donor and recipient and are autocytotoxic lymphocytes which can produce acute graft versus host disease in recipients of identical twin transplants. The cessation of acute graft versus host disease occurs when suppressor lymphocytes appear in the recipient's peripheral circulation. Chronic graft versus host disease is produced by immunocompetent lymphocytes that differentiate in the recipient. Its control is unknown. Some patients with chronic graft versus host disease have in vivo activated suppressor lymphocytes which produce a secondary immunoincompetence and an increased susceptibility to bacterial sepsis and death.
人类移植物抗宿主病由两种不同的临床实体组成，即急性移植物抗宿主病和慢性移植物抗宿主病，它们具有不同的发病机制。急性移植物抗宿主病是由供体免疫活性T淋巴细胞或裸淋巴细胞攻击受体组织相容性抗原所致。裸淋巴细胞可能攻击供体和受体共有的抗原，并且是自身细胞毒性淋巴细胞，可在同卵双胞胎移植受体中引发急性移植物抗宿主病。当抑制性淋巴细胞出现在受体外周循环中时，急性移植物抗宿主病就会停止。慢性移植物抗宿主病是由在受体中分化的免疫活性淋巴细胞引起的。其控制机制尚不清楚。一些慢性移植物抗宿主病患者体内存在活化的抑制性淋巴细胞，这些细胞会导致继发性免疫无能，并增加对细菌性败血症和死亡的易感性。
