研究人员发现，阻断肺部里的一种免疫细胞蛋白质LIGHT，能预防哮喘模式小鼠的呼吸道重构，新成果发表在4月在线出版的《自然—医学》期刊上。这项研究显现，以该通道为靶标可预防与哮喘有关的呼吸道重构所带来的呼吸问题。
严重哮喘患者在其肺部有慢性未解决的炎症，这种炎症导致呼吸道重构、纤维化，肺功能被降低。尽管目前治疗哮喘的方法能控制呼吸道炎症，但却基本上不能影响呼吸道的重构。
Michael Croft和同事发现，当免疫细胞因暴露于屋尘螨而被激活时，蛋白质LIGHT也被表达出来，并导致呼吸道重构。通过基因和抗体调控阻断LIGHT的表达，就能在暴露于过敏原时预防呼吸道重构和肺功能的降低。（生物谷Bioon.com）
生物谷推荐原文：
Nature Medicine DOI:10.1038/nm.2356
The tumor necrosis factor family member LIGHT is a target for asthmatic airway remodeling
Taylor A Doherty; Pejman Soroosh; Naseem Khorram; Satoshi Fukuyama; Peter Rosenthal; Jae Youn Cho; Paula S Norris; Heonsik Choi; Stefanie Scheu; Klaus Pfeffer; Bruce L Zuraw; Carl F Ware; David H Broide; Michael Croft
Individuals with chronic asthma show a progressive decline in lung function that is thought to be due to structural remodeling of the airways characterized by subepithelial fibrosis and smooth muscle hyperplasia. Here we show that the tumor necrosis factor (TNF) family member LIGHT is expressed on lung inflammatory cells after allergen exposure. Pharmacological inhibition of LIGHT using a fusion protein between the IgG Fc domain and lymphotoxin β receptor (LTβR) reduces lung fibrosis, smooth muscle hyperplasia and airway hyperresponsiveness in mouse models of chronic asthma, despite having little effect on airway eosinophilia. LIGHT-deficient mice also show a similar impairment in fibrosis and smooth muscle accumulation. Blockade of LIGHT suppresses expression of lung transforming growth factor-β (TGF-β) and interleukin-13 (IL-13), cytokines implicated in remodeling in humans, whereas exogenous administration of LIGHT to the airways induces fibrosis and smooth muscle hyperplasia, Thus, LIGHT may be targeted to prevent asthma-related airway remodeling.
