IL-23-induced macrophage polarization and its pathological roles in mice with imiquimod-induced psoriasis.
IL-23-induced macrophage polarization and its pathological roles in mice with imiquimod-induced psoriasis.
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IL-23 诱导的巨噬细胞极化及其在咪喹莫特诱导的银屑病小鼠中的病理作用。
DOI：
10.1007/s13238-018-0505-z
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发表时间：
2018-12
期刊：
影响因子：
21.1
通讯作者：
Zhao Y
中科院分区：
文献类型：
--
作者：
Hou Y;Zhu L;Tian H;Sun HX;Wang R;Zhang L;Zhao Y
巨噬细胞在组织应激和炎症反应期间获得不同的表型。巨噬细胞大致分为两个不同的亚群，称为炎症M1和抗炎M2巨噬细胞。我们在此鉴定了由IL-23驱动的独特的致病性巨噬细胞亚群，其具有不同的基因表达谱，包括确定类型的细胞因子。用不同的细胞因子体外刺激新鲜分离的静息状态小鼠腹腔巨噬细胞，采用基因芯片、实时荧光定量PCR、ELISA和多色流式细胞术检测细胞因子和趋化因子的表达。使用巨噬细胞的连续转移和咪喹莫特诱导的银屑病小鼠。与M1和M2极化的巨噬细胞相反，IL-23处理的巨噬细胞产生大量的IL-17 A、IL-22和IFN-γ。生物化学和分子生物学研究表明，IL-23通过信号转导和转录激活因子3（STAT 3）-维甲酸相关孤儿受体-γ T（RORγT）途径诱导巨噬细胞表达IL-17 A。T-bet介导IL-23处理的巨噬细胞中IFN-γ的产生。重要的是，IL-23处理的巨噬细胞显著促进银屑病样小鼠模型中的皮炎发病机制。与M1和M2巨噬细胞相比，IL-23处理的静息巨噬细胞表达独特的基因表达prolife。IL-23诱导的巨噬细胞极化的鉴定可能有助于我们理解巨噬细胞亚群在Th 17细胞因子相关发病机制中的作用。本文的在线版本（10.1007/s13238-018-0505-z）包含补充材料，可供授权用户使用。
Macrophages acquire distinct phenotypes during tissue stress and inflammatory responses. Macrophages are roughly categorized into two different subsets named inflammatory M1 and anti-inflammatory M2 macrophages. We herein identified a unique pathogenic macrophage subpopulation driven by IL-23 with a distinct gene expression profile including defined types of cytokines. The freshly isolated resting mouse peritoneal macrophages were stimulated with different cytokines in vitro, the expression of cytokines and chemokines were detected by microarray, real-time PCR, ELISA and multiple colors flow cytometry. Adoptive transfer of macrophages and imiquimod-induced psoriasis mice were used. In contrast to M1- and M2-polarized macrophages, IL-23-treated macrophages produce large amounts of IL-17A, IL-22 and IFN-γ. Biochemical and molecular studies showed that IL-23 induces IL-17A expression in macrophages through the signal transducer and activator of transcription 3 (STAT3)-retinoid related orphan receptor-γ T (RORγT) pathway. T-bet mediates the IFN-γ production in IL-23-treated macrophages. Importantly, IL-23-treated macrophages significantly promote the dermatitis pathogenesis in a psoriasis-like mouse model. IL-23-treated resting macrophages express a distinctive gene expression prolife compared with M1 and M2 macrophages. The identification of IL-23-induced macrophage polarization may help us to understand the contribution of macrophage subpopulation in Th17-cytokines-related pathogenesis. The online version of this article (10.1007/s13238-018-0505-z) contains supplementary material, which is available to authorized users.
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影响因子：
64.8
作者：
Cella, Marina;Fuchs, Anja;Vermi, William;Facchetti, Fabio;Otero, Karel;Lennerz, Jochen K. M.;Doherty, Jason M.;Mills, Jason C.;Colonna, Marco
通讯作者：
Colonna, Marco
DOI：
10.1056/nejmoa1612197
发表时间：
2017-03-23
期刊：
The New England journal of medicine
影响因子：
--
作者：
Moutsopoulos NM;Zerbe CS;Wild T;Dutzan N;Brenchley L;DiPasquale G;Uzel G;Axelrod KC;Lisco A;Notarangelo LD;Hajishengallis G;Notarangelo LD;Holland SM
通讯作者：
Holland SM
影响因子：
56.9
作者：
Duerr, Richard H.;Taylor, Kent D.;Cho, Judy H.
通讯作者：
Cho, Judy H.
DOI：
10.1038/nri3073
发表时间：
2011-10-14
期刊：
Nature reviews. Immunology
影响因子：
--
作者：
通讯作者：
--
影响因子：
4.4
作者：
Hou, Yuzhu;Lin, Haijiang;Zhao, Yong
通讯作者：
Zhao, Yong