Nonclassical Ly6C(-) monocytes drive the development of inflammatory arthritis in mice.
Nonclassical Ly6C(-) monocytes drive the development of inflammatory arthritis in mice.
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DOI：
10.1016/j.celrep.2014.09.032
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发表时间：
2014-10-23
期刊：
影响因子：
8.8
通讯作者：
Perlman H
中科院分区：
文献类型：
--
作者：
Misharin AV;Cuda CM;Saber R;Turner JD;Gierut AK;Haines GK 3rd;Berdnikovs S;Filer A;Clark AR;Buckley CD;Mutlu GM;Budinger GR;Perlman H
单核细胞和巨噬细胞的不同亚群和/或极化表型可能在炎症的发生和消退过程中发挥不同的作用。在这里，我们在类风湿性关节炎的小鼠模型中证明，无菌关节炎症的发生和发展需要非经典Ly6C -单核细胞。此外，非经典Ly6C -单核细胞分化为炎性巨噬细胞（M1），其驱动疾病的发病机制并在消退期表现出可塑性。在关节炎的发展过程中，这些细胞向交替激活表型（M2）极化，促进关节炎症的解决。Ly6C -单核细胞的涌入及其随后的经典活化和交替活化发生在滑膜组织内的巨噬细胞中，而这些巨噬细胞在整个关节炎过程中表达M2极化标记物，并在初始阶段减轻关节炎症。这些数据表明，损伤后募集到关节的循环Ly6C -单核细胞协调了自身免疫性关节炎症的发展和消退。
Different subsets and/or polarized phenotypes of monocytes and macrophages may play distinct roles during the development and resolution of inflammation. Here, we demonstrate in a murine model of rheumatoid arthritis that non-classical Ly6C− monocytes are required for the initiation and progression of sterile joint inflammation. Moreover, non-classical Ly6C− monocytes differentiate into inflammatory macrophages (M1), which drive disease pathogenesis and display plasticity during the resolution phase. During the development of arthritis, these cells polarize toward an alternatively activated phenotype (M2), promoting the resolution of joint inflammation. The influx of Ly6C− monocytes and their subsequent classical and then alternative activation occurs without changes in synovial tissue-resident macrophages, which express markers of M2 polarization throughout the course of the arthritis and attenuate joint inflammation during the initiation phase. These data suggest that circulating Ly6C− monocytes recruited to the joint upon injury orchestrate the development and resolution of autoimmune joint inflammation.
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DOI：
10.1126/science.1247651
发表时间：
2014-02-14
期刊：
Science (New York, N.Y.)
影响因子：
--
作者：
Jaitin DA;Kenigsberg E;Keren-Shaul H;Elefant N;Paul F;Zaretsky I;Mildner A;Cohen N;Jung S;Tanay A;Amit I
通讯作者：
Amit I
影响因子：
30.5
作者：
通讯作者：
--
影响因子：
5.3
作者：
Jung, S;Aliberti, J;Littman, DR
通讯作者：
Littman, DR
影响因子：
20.1
作者：
Hamers, Anouk A. J.;Vos, Mariska;de Vries, Carlie J. M.
通讯作者：
de Vries, Carlie J. M.
影响因子：
7.3
作者：
Korns D;Frasch SC;Fernandez-Boyanapalli R;Henson PM;Bratton DL
通讯作者：
Bratton DL