The role of the innate immune system in lung allograft rejection


Journal Article (Review)

Purpose of review: The long-term survival after lung transplantation is limited by high rates of lung allograft rejection. Although innate immunity is central to pulmonary host defense, its role in transplantation biology has been previously unstudied. In this review the authors highlight recent studies that suggest innate immune mechanisms potentially contribute to the high rates of pulmonary allograft rejection. Recent findings: An increasing body of evidence suggests that the innate immune system critically regulates the development of allograft rejection in a number of solid organ transplants. Components of the innate immune system including both cell surface and soluble pattern recognition receptors modulate phagocytosis of pathogens, antigen presentation, and host adaptive immune responses. Polymorphisms have been identified in genes that encode components of the innate immune system leading to functional differences in innate responsiveness. This review summarizes the recent literature that implicates toll-like receptors, collectins, and defensins in the development of allograft rejection. For example, recent clinical studies suggest that genetic polymorphisms in toll-like receptor-4 associated with blunted innate immune signaling are a key determinant in long-term outcomes after lung transplant. Summary: Understanding the role of the innate immune system in the pathogenesis of acute and chronic allograft rejection after lung transplantation will enhance our understanding of transplant biology and potentially lead to the identification of new therapeutic targets. Future drugs that target novel immune pathways are critical to the development of more effective immunosuppressive strategies necessary for successful long-term lung transplant outcomes. © 2005 Lippincott Williams & Wilkins.

Full Text

Duke Authors

Cited Authors

  • Zaas, DW; Palmer, SM

Published Date

  • September 1, 2005

Published In

Volume / Issue

  • 10 / 3

Start / End Page

  • 221 - 226

International Standard Serial Number (ISSN)

  • 1087-2418

Digital Object Identifier (DOI)

  • 10.1097/01.mot.0000169370.30637.4a

Citation Source

  • Scopus