Sullivan K M, Parkman R
Clin Haematol. 1983 Oct;12(3):775-89. doi: 10.1016/s0308-2261(83)80010-1.
Acute and chronic GVHD remain major impediments to the wider application of allogeneic marrow transplantation. It is presumed that human acute GVHD is analogous to the murine model which is initiated by donor T lymphocytes reacting with recipient 'minor' histocompatibility antigens. Chronic GVHD may result from immunoaggression of donor lymphoid cells that have developed and differentiated within the host. Lack of GVHD (i.e., the development of tolerance) may be due either to generation within the host of specific suppressor lymphocytes or to clonal deletion of alloreactive donor cells. Over the last five years progress has been made in the recognition, early diagnosis and successful therapy of chronic GVHD. Methods of prevention and therapy of acute GVHD are still largely unsuccessful. With improved understanding of immune regulation, it is hoped that GVHD can be eliminated in patients transplanted for non-malignant conditions and adroitly modified (without loss of anti-leukaemic potential) in patients with malignant disorders. The challenge of the coming decade is to reach these goals while speeding the return of full immunological competence in the marrow transplant recipient.
急性和慢性移植物抗宿主病（GVHD）仍然是异体骨髓移植广泛应用的主要障碍。据推测，人类急性GVHD类似于小鼠模型，由供体T淋巴细胞与受体“次要”组织相容性抗原反应引发。慢性GVHD可能源于在宿主体内发育和分化的供体淋巴细胞的免疫攻击。缺乏GVHD（即耐受性的发展）可能是由于宿主体内产生了特异性抑制淋巴细胞，或者是由于同种反应性供体细胞的克隆缺失。在过去五年中，在慢性GVHD的识别、早期诊断和成功治疗方面取得了进展。急性GVHD的预防和治疗方法在很大程度上仍然不成功。随着对免疫调节的进一步了解，希望在非恶性疾病患者的移植中消除GVHD，并在恶性疾病患者中巧妙地加以调整（同时不丧失抗白血病潜力）。未来十年的挑战是在加速骨髓移植受者完全免疫能力恢复的同时实现这些目标。
