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The CD200-CD200R axis in local control of lunj inflammation

机译:CD200-CD200R轴在局部控制肺部炎症

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The epithelial surfaces of the lungs and airways provide a fragile interface between the immune system and the external environment rich in microbial and nonmicrobial stimuli. Fine control of immunological homeostasis in this unique microenvironment is central to survival, as maintenance of local tissue integrity is obligatory for efficient gas exchange. The ever-present danger is excessively intense or prolonged host defense, particularly against viral infections that often penetrate to the lower respiratory tract. How the local immune system routinely achieves successful elimination of such infections without triggering the influenza-like symptoms that are the hallmark of excessively vigorous host responses has puzzled successive generations of researchers. In this issue of Nature Immunology, Hussell and colleagues present challenging new findings from a mouse influenza model that stem from the primary observation that infected Cd200(~/~) mice, which are deficient in the negative regulator CD200, have much more pulmonary alveolar macrophage (PAM) activity, which leads to death or delayed resolution of airway inflammation
机译:肺和气道的上皮表面在免疫系统与富含微生物和非微生物刺激的外部环境之间提供了脆弱的界面。在这种独特的微环境中,对免疫稳态的精细控制对于生存至关重要,因为必须维持局部组织的完整性才能进行有效的气体交换。永远存在的危险是过度密集或长时间的宿主防御,特别是对于经常渗透到下呼吸道的病毒感染。本地免疫系统如何在不引发流感样症状的情况下常规成功消除此类感染,而流感样症状是宿主反应过度剧烈的特征,这困扰了历代研究人员。在本期《自然免疫学》中,Hussell及其同事从小鼠流感模型中提出了具有挑战性的新发现,该发现源自以下初步观察结果:受感染的Cd200(〜/〜)小鼠(其负调节剂CD200不足)具有更多的肺泡巨噬细胞(PAM)活动,导致呼吸道炎症死亡或延迟解决

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