Iwasaki Tsuyoshi
Division of Rheumatology and Clinical Immunology, Department of Internal Medicine, Hyogo College of Medicine, Nishinomiya, Hyogo, Japan.
Clin Med Res. 2004 Nov;2(4):243-52. doi: 10.3121/cmr.2.4.243.
Graft-versus-host disease (GVHD) is a lethal complication of allogeneic hematopoietic stem cell transplantation (HSCT) where immunocompetent donor T cells attack the genetically disparate host cells. The predominant symptoms of acute GVHD occur in the skin, liver, and intestine. Induction of acute GVHD can be divided into three phases: recipient conditioning, donor T cell activation, and effector cell-mediated GVHD. Chronic GVHD usually appears up to 100 days after HSCT and is characterized by symptoms similar to those observed for autoimmune disease. It is possible that chronic GVHD is the result of autoreactive T cells that escaped negative selection due to damage to the thymus from conditioning regimens, acute GVHD, and/or age related atrophy. Recent advances in the understanding of the basic mechanisms involved in GVHD pathophysiology have led to new strategies designed to block GVHD. This review focuses on recent developments in the treatment of GVHD, including insights gained from our own experimental studies.
移植物抗宿主病(GVHD)是异基因造血干细胞移植(HSCT)的一种致命并发症,在此过程中,具有免疫活性的供体T细胞会攻击基因不同的宿主细胞。急性GVHD的主要症状出现在皮肤、肝脏和肠道。急性GVHD的诱发可分为三个阶段:受体预处理、供体T细胞活化和效应细胞介导的GVHD。慢性GVHD通常在HSCT后100天内出现,其特征是出现与自身免疫性疾病类似的症状。慢性GVHD可能是由于预处理方案、急性GVHD和/或年龄相关萎缩对胸腺造成损伤,导致自身反应性T细胞逃脱阴性选择的结果。对GVHD病理生理学基本机制认识的最新进展催生了旨在阻断GVHD的新策略。本综述重点关注GVHD治疗的最新进展,包括我们自己的实验研究获得的见解。