Puliaev R A, Puliaeva I A, Ryan A E, Via C S
Pathology Department, Uniformed Services University of Health Sciences, Bethesda, MD 20814, USA.
Curr Med Chem Immunol Endocr Metab Agents. 2005 Dec 1;5(6):575-583. doi: 10.2174/156801305774962204.
Since its description roughly 30 years ago, the parent-into-F1 model of graft-vs.-host disease has provided insights into the mechanisms of in vivo T cell activation and the pathogenesis of autoimmune conditions. A new and emerging role for the P-->F1 model is one of identifying agents with immunomodulatory activity and defining in vivo mechanisms that promote cell mediated or antibody mediated immune responses. Because F1 mice are not irradiated prior to donor cell transfer, the P-->F1 model has in the past not been strictly analogous to human hematopoetic stem cell transplantation. However with the advent of newer non-myeloablative conditioning regimens, the model may assume more relevance. In this article, we first provide a review of relevant earlier fundamental observations followed by a summary of recent work from our laboratory in which acute and chronic GVHD in this model have been used not only to study normal T cell responses in vivo but also to define mechanisms important in the pathogenesis of autoimmunity and immunomodulation.
大约30年前首次被描述以来，亲代到F1子代的移植物抗宿主病模型为体内T细胞活化机制及自身免疫性疾病的发病机制提供了深入见解。P→F1模型一个新出现的作用是识别具有免疫调节活性的药物，并确定促进细胞介导或抗体介导免疫反应的体内机制。由于在供体细胞移植前未对F1小鼠进行照射，过去P→F1模型与人类造血干细胞移植并不严格相似。然而，随着更新的非清髓性预处理方案的出现，该模型可能具有更大的相关性。在本文中，我们首先回顾相关的早期基础观察结果，然后总结我们实验室最近的工作，其中该模型中的急性和慢性移植物抗宿主病不仅用于研究体内正常T细胞反应，还用于确定自身免疫发病机制和免疫调节中重要的机制。
