Nature Immunology：肺部组织通过免疫调控保护自己

在7月出版的《自然—免疫学》期刊上，科学家们揭示了一个秘密：肺部组织在对付空气中的刺激物或感染物时，如何避免让自己受到过度损害。对因呼吸道感染而发生并发症的患者来说，新发现非常有助于开发新治疗方法。
肺是非常精致的组织，常常会暴露在通过呼吸进入的各种微生物和微颗粒中。过度的免疫反应会导致疤痕，影响肺气体交换功能。
英国伦敦帝国理工学院Tracy Hussell和同事报告说，一种名为CD200R的分子会向停留在肺部的特定免疫分子施加一种抑制作用，提高肺部需要免疫细胞的门槛。一旦这种反应被启动后，CD200R就会减少肺部的感染，缓解对肺组织的损伤。在受到流感病毒感染时，缺乏CD200R的小鼠的存活率更低。死亡原因是不受限制的免疫细胞对间接组织造成了过度损伤。（生物谷Bioon.com）
生物谷推荐原始出处：
Nature Immunology，doi : 10.1038/ni.1637，Robert J Snelgrove，Tracy Hussell
A critical function for CD200 in lung immune homeostasis and the severity of influenza infection
Robert J Snelgrove1, John Goulding1, Arnaud M Didierlaurent1, Daphne Lyonga1, Seema Vekaria1, Lorna Edwards1, Emily Gwyer1, Jonathon D Sedgwick2, A Neil Barclay3 & Tracy Hussell1
AbstractThe lung must maintain a high threshold of immune 'ignorance' to innocuous antigens to avoid inflammatory disease that depends on the balance of positive inflammatory signals and repressor pathways. We demonstrate here that airway macrophages had higher expression of the negative regulator CD200 receptor (CD200R) than did their systemic counterparts. Lung macrophages were restrained by CD200 expressed on airway epithelium. Mice lacking CD200 had more macrophage activity and enhanced sensitivity to influenza infection, which led to delayed resolution of inflammation and, ultimately, death. The administration of agonists that bind CD200R, however, prevented inflammatory lung disease. Thus, CD200R is critical for lung macrophage immune homeostasis in the resting state and limits inflammatory amplitude and duration during pulmonary influenza infection.
1 Imperial College London, Kennedy Institute, London, W6 8LH, UK.2 Eli Lilly, Indianapolis 46285, USA.3 Sir William Dunn School of Pathology, University of Oxford, Oxford OX1 3RE, UK.