The pulmonary collectins, SP-A and SP-D, orchestrate innate immunity in the lung.
The pulmonary collectins, SP-A and SP-D, orchestrate innate immunity in the lung.
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DOI：
10.1172/jci15293
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发表时间：
2002-03
期刊：
影响因子：
--
通讯作者：
F. McCormack;J. Whitsett
中科院分区：
文献类型：
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作者：
F. McCormack;J. Whitsett
这里提供的数据表明 SP-A 和 SP-D 在肺部发挥着独特且互补的宿主防御功能。尽管这两种蛋白质都是凝集素、调理素和炎症免疫调节剂，但它们与各种病原体和炎症细胞的相互作用是独特的。例如，SP-A 和 SP-D 似乎对结核分枝杆菌的吞噬作用和肺泡巨噬细胞氧化反应的调节具有相反的作用。肺集合素在气道内壁划分成不同的微区； SP-D 似乎更喜欢 ALL 的水相，但可能与上皮细胞表面的关联较弱，而 SP-A 富含肾小管髓磷脂和表面活性剂膜界面。虽然最初的观点认为，表面活性剂的调节和功能需要管状髓磷脂，但现在看来，它更有可能作为固相、高密度 SP-A 阵列发挥主要的宿主防御作用，优化表面活性剂的表面特性，并在气肺界面拦截吸入的微生物。
The data presented here suggest that SP-A and SP-D perform distinct, as well as complementary, host defense functions in the lung. Although both proteins are agglutinins, opsonins, and inflammatory immunomodulators, they interact uniquely with various pathogens and inflammatory cells. For instance, SP-A and SP-D appear to have opposite effects on the phagocytosis of Mycobacterium tuberculosis and on regulation of oxidant responses from alveolar macrophages. The pulmonary collectins partition into different microdomains within the airway lining; SP-D appears to prefer the aqueous phase of the ALL but may be weakly associated with the surface of epithelial cells, whereas SP-A is enriched in tubular myelin and at surfactant membrane interfaces. While the initial view held that tubular myelin would be required for surfactant regulation and function, it now appears more likely that it serves a primary host defense role as a solid-phase, high-density SP-A array that optimizes the surface properties of surfactant and the interception of inhaled microbes at the air-lung interface.