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首页> 外文期刊>Human Immunology: Official Journal of the American Society for Histocompatibility and Immunogenetics >Attenuated expression of interferon-β and interferon-λ1 by human alternatively activated macrophages
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Attenuated expression of interferon-β and interferon-λ1 by human alternatively activated macrophages

机译：人交替激活的巨噬细胞对干扰素-β和干扰素-λ1的减弱表达

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摘要

Macrophages can be polarized into classically (CAM) or alternatively (AAM) activated macrophages with IFN-γ or IL-4, respectively. CAM are associated with type 1 immune responses and are implicated in autoimmunity; AAM are associated with type 2 responses and are implicated in allergic diseases. An impediment in investigating macrophage biology using primary human monocyte derived macrophages is the wide inter-donor heterogeneity and the limited quantity of cells that survive in vitro polarization. To overcome this impediment, we established a protocol to generate CAM and AAM cultures derived from the THP-1 human promonocytic cell line. In this report, we demonstrate that THP-CAM and -AAM express gene and protein markers that define their primary human monocyte derived counterparts, such as IL-1β, CXCL10, and CXCL11 for CAM, and MRC1, IL-4 and CCL22 for AAM. In addition, we demonstrate that STAT6 is selectively activated in THP-AAM which, upon LPS stimulation, have an attenuated or delayed expression of IFN-β, IFN-λ1, and IFN α/β pathway genes compared to their CAM counterparts. Taken together, these findings may help further investigate human diseases associated with the alternatively activated macrophage phenotype using this reproducible in vitro macrophage model.
机译：巨噬细胞可以极化成分别具有IFN-γ或IL-4的经典（CAM）或替代（AAM）活化的巨噬细胞。 CAM与1型免疫反应有关，并与自身免疫有关。 AAM与2型反应相关，并与过敏性疾病有关。使用原代人单核细胞衍生的巨噬细胞研究巨噬细胞生物学的一个障碍是供体间异质性很广，并且在体外极化中存活的细胞数量有限。为了克服这一障碍，我们建立了一个协议来生成源自THP-1人原单核细胞系的CAM和AAM培养物。在本报告中，我们证明THP-CAM和-AAM表达定义其主要人类单核细胞衍生对应物的基因和蛋白质标记，例如CAM的IL-1β，CXCL10和CXCL11，以及AAM的MRC1，IL-4和CCL22 。此外，我们证明STAT6在THP-AAM中被选择性激活，与CAM对应物相比，LPS刺激后STAT6具有减弱或延迟的IFN-β，IFN-λ1和IFNα/β通路基因表达。综上所述，这些发现可能有助于进一步利用这种可复制的体外巨噬细胞模型研究与交替激活的巨噬细胞表型相关的人类疾病。

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