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肺移植排斥反应的免疫机制。

Immune mechanisms of lung allograft rejection.

作者信息

Snyder Laurie D, Palmer Scott M

机构信息

Department of Medicine, Division of Pulmonary and Critical Care Medicine, Duke University Medical Center, Durham, North Carolina 27710, USA.

出版信息

Semin Respir Crit Care Med. 2006 Oct;27(5):534-43. doi: 10.1055/s-2006-954610.

Abstract

Extended survival after lung transplantation is primarily limited by progressive airflow obstruction and fibrotic obliteration of the small airways, termed bronchiolitis obliterans syndrome (BOS) and bronchiolitis obliterans (BO), respectively. BO is thought to represent the pulmonary-specific manifestation of chronic allograft rejection and the end result of a spectrum of different immunological insults to the allograft. Historically, research has focused on the adaptive immune system and its cellular-based rejection as the driving factor in the development of BO. Recent research in animal lung transplant models and human lung transplant recipients has identified that chemokines, humoral immunity, autoimmunity, and innate immunity also contribute to lung allograft rejection and BO. This review explores the complex immunological mechanisms that promote the high rate of pulmonary allograft failure and significantly impair survival after lung transplantation. We also identify areas for further research critical to improving transplant outcomes.

摘要

肺移植术后长期存活主要受进行性气流阻塞和小气道纤维化闭塞的限制,分别称为闭塞性细支气管炎综合征(BOS)和闭塞性细支气管炎(BO)。BO被认为是慢性移植物排斥反应的肺部特异性表现,也是同种异体移植物受到一系列不同免疫损伤的最终结果。从历史上看,研究主要集中在适应性免疫系统及其基于细胞的排斥反应,将其作为BO发生发展的驱动因素。最近在动物肺移植模型和人类肺移植受者中的研究发现,趋化因子、体液免疫、自身免疫和固有免疫也参与了肺同种异体移植物排斥反应和BO的发生。本综述探讨了促进肺同种异体移植物高失败率并显著损害肺移植术后存活的复杂免疫机制。我们还确定了对改善移植结果至关重要的进一步研究领域。

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