Update on the role of alternatively activated macrophages in asthma.
Update on the role of alternatively activated macrophages in asthma.
复制标题
替代激活巨噬细胞在哮喘中作用的最新进展
DOI：
10.2147/jaa.s104508
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发表时间：
2016
影响因子：
3.2
通讯作者：
Zhu L
中科院分区：
文献类型：
--
作者：
Jiang Z;Zhu L
在过敏性气道炎症反应中，肺巨噬细胞连接先天性和适应性免疫反应。肺泡巨噬细胞（Alveolar macrophages, AMs）和间质巨噬细胞是两种不同的表型，在生理和病理条件下发挥不同的免疫功能。暴露于病原体诱导AM细胞极化为经典活化的巨噬细胞（M1细胞）和交替活化的巨噬细胞（M2细胞）。M1细胞主要表达促炎细胞因子如TNF-α和IL-1 β，诱导肺部炎症和组织损伤。M2细胞进一步分为M2a和M2c亚群。M2a细胞主要产生过敏性细胞因子IL-4和IL-13，而M2c细胞主要产生抗炎细胞因子IL-10。在哮喘的不同阶段，M2a和M2c细胞参与起始、炎症消退和组织重塑的过程是不同的。微环境动态影响AM细胞的极化。细胞因子、趋化因子和免疫调节细胞相互作用，影响M1和M2细胞极化之间的平衡，从而影响疾病进展。因此，通过分子干预调节AM表型在治疗哮喘和其他过敏性炎症疾病方面具有治疗潜力。本文综述了这些巨噬细胞亚型极化和功能特化的最新进展，重点介绍了哮喘患者和动物模型中M2细胞极化的调节。
Lung macrophages link innate and adaptive immune responses during allergic airway inflammatory responses. Alveolar macrophages (AMs) and interstitial macrophages are two different phenotypes that differentially exert immunological function under physiological and pathological conditions. Exposure to pathogen induces polarization of AM cells into classically activated macrophages (M1 cells) and alternatively activated macrophages (M2 cells). M1 cells dominantly express proinflammatory cytokines such as TNF-α and IL-1 β and induce lung inflammation and tissue damage. M2 cells are further divided into M2a and M2c subsets. M2a cells dominantly produce allergic cytokines IL-4 and IL-13, but M2c cells dominantly produce anti-inflammatory cytokine IL-10. M2a and M2c cells are differently involved in initiation, inflammation resolution, and tissue remodeling in the different stages of asthma. Microenvironment dynamically influences polarization of AM cells. Cytokines, chemokines, and immune-regulatory cells interplay and affect the balance between the polarization of M1 and M2 cells, subsequently influencing disease progression. Thus, modulation of AM phenotypes through molecular intervention has therapeutic potential in the treatment of asthma and other allergic inflammatory diseases. This review updated recent advances in polarization and functional specialization of these macrophage subtypes with emphasis on modulation of polarization of M2 cells in asthma of human subjects and animal models.