在7月出版的《自然—免疫學(xué)》期刊上,，科學(xué)家們揭示了一個秘密：肺部組織在對付空氣中的刺激物或感染物時，如何避免讓自己受到過度損害,。對因呼吸道感染而發(fā)生并發(fā)癥的患者來說,，新發(fā)現(xiàn)非常有助于開發(fā)新治療方法。
肺是非常精致的組織,，常常會暴露在通過呼吸進入的各種微生物和微顆粒中,。過度的免疫反應(yīng)會導(dǎo)致疤痕，影響肺氣體交換功能,。
英國倫敦帝國理工學(xué)院Tracy Hussell和同事報告說,，一種名為CD200R的分子會向停留在肺部的特定免疫分子施加一種抑制作用，提高肺部需要免疫細胞的門檻,。一旦這種反應(yīng)被啟動后,，CD200R就會減少肺部的感染，緩解對肺組織的損傷,。在受到流感病毒感染時,，缺乏CD200R的小鼠的存活率更低。死亡原因是不受限制的免疫細胞對間接組織造成了過度損傷,。（生物谷Bioon.com）
生物谷推薦原始出處：
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.
