趋化因子
肺纤维化
细胞因子
CCL17型
信号转导
特发性肺纤维化
纤维化
细胞生物学
肺泡巨噬细胞
免疫学
生物
癌症研究
巨噬细胞
炎症
肺
医学
病理
体外
CXCL10型
内科学
生物化学
作者
Dmitri V. Pechkovsky,Antje Prasse,Florian Kollert,Kathrin M. Engel,Jan Dentler,Werner Luttmann,Karlheinz Friedrich,Joachim Müller–Quernheim,Gernot Zissel
标识
DOI:10.1016/j.clim.2010.06.017
摘要
Activated macrophages have been characterized as M1 and M2 according to their inflammatory response pattern. Here we analyzed the M2 marker expression and intracellular signal transduction in the course of cytokine-driven differentiation. We found elevated spontaneous production of the chemokines CCL17, CCL18 and CCL22 and increased expression of CD206 by alveolar macrophages from patients with lung fibrosis. Stimulation of normal human AM with Th2 cytokines IL-4 and/or IL-10 in vitro revealed IL-4 as the most powerful inducer of M2-phenotype in AM and monocytes. Importantly, IL-10 enhanced IL-4-induced expression of CCL18 and IL-1RA in a synergistic fashion. IL-4/IL-10 stimulation induces a strong activation of STAT3 in AM from fibrosis patients. These results suggest an important role for M2 polarized AM in the pathogenesis of pulmonary fibrosis and indicate that both IL-4 and IL-10 account for human AM phenotype shift to M2, as seen in patients with fibrotic interstitial lung diseases.
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