期刊
JOURNAL OF EXPERIMENTAL MEDICINE
卷 202, 期 1, 页码 97-110出版社
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.20042481
关键词
-
资金
- NHLBI NIH HHS [K08 HL072775] Funding Source: Medline
- NIAID NIH HHS [R01 AI050892, K08 AI055663] Funding Source: Medline
Leukotriene B 4 is a lipid mediator that recently has been shown to have potent chemotactic activity for effector T lymphocytes mediated through its receptor, BLT1. Here, we developed a novel murine model of acute lung rejection to demonstrate that BLT1 controls effector CD8(+) T cell trafficking into the lung and that disruption of BLT1 signaling in CD8(+) T cells reduces lung inflammation and mortality in the model. In addition, we used BLT1-deficient mice and a BLT1 antagonist in two tracheal transplant models of lung transplantation to demonstrate the importance of BLT1 for the recruitment of T cells into tracheal allografts. We also show that BLT1-mediated CD8(+) T cell recruitment plays an important role in the development of airway fibroproliferation and obliteration. Finally, in human studies of lung transplant recipients, we found that BLT1 is up-regulated on T lymphocytes isolated from the airways of patients with obliterative bronchiolitis. These data demonstrate that BLT1 contributes to the development of lung rejection and obliterative bronchiolitis by mediating effector T lymphocyte trafficking into the lung. This is the first report that describes a pathologic role for BLT1-mediated T lymphocyte recruitment in disease and identifies BLT1 as a potential therapeutic target after lung transplantation.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据