CX3CL1/fractalkine regulates the differentiation of human peripheral blood monocytes and monocyte-derived dendritic cells into osteoclasts
CX3CL1/fractalkine regulates the differentiation of human peripheral blood monocytes and monocyte-derived dendritic cells into osteoclasts
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CX3CL1/fractalkine调节人外周血单核细胞和单核细胞源性树突状细胞向破骨细胞的分化
DOI：
10.1016/j.cyto.2021.155652
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发表时间：
2021
期刊：
影响因子：
3.8
通讯作者：
Nanki Toshihiro
中科院分区：
文献类型：
--
作者：
Muraoka Sei;Kaneko Kaichi;Motomura Kaori;Nishio Junko;Nanki Toshihiro
破骨细胞分化在炎症条件下促进，并且破骨细胞在类风湿性关节炎（RA）的骨破坏中起主要作用。趋化因子（C-X3-C基序）配体1（CX 3CL 1），也称为fractalkine，作为一种化学引诱物和粘附分子，并参与RA的发病机制。CX 3CL 1的阻断抑制巨噬细胞和破骨细胞前体细胞迁移到发炎的滑膜中。在本研究中，我们研究了CX 3CL 1对人外周血单核细胞和单核细胞来源的树突状细胞的破骨细胞分化的直接刺激作用。CX 3CL 1刺激显著促进了CD 16-单核细胞和单核细胞衍生的树突状细胞由巨噬细胞集落刺激因子（M-CSF）和NF-κB配体受体激活剂（RANKL）诱导的破骨细胞分化。另一方面，用M-CSF和RANKL处理的CD 16+单核细胞不分化成破骨细胞，即使用CX 3CL 1也是如此。钙吸收显着增加单核细胞衍生的破骨细胞，但不是树突状细胞衍生的破骨细胞，加入CX 3CL 1。目前的结果表明，CX 3CL 1直接调节破骨细胞分化。CX 3CL 1可能在RA的发病机制中发挥重要作用，不仅通过炎症细胞的积累，而且通过破骨细胞的生成。
Osteoclast differentiation is promoted under inflammatory conditions and osteoclasts play a major role in bone destruction in rheumatoid arthritis (RA). Chemokine (C-X3-C motif) ligand 1 (CX3CL1), also known as fractalkine, functions as a chemoattractant and adhesion molecule, and is involved in the pathogenesis of RA. The blockade of CX3CL1 inhibits the migration of macrophages and osteoclast precursor cells into the inflamed synovium. In the present study, we investigated the direct stimulatory effects of CX3CL1 on osteoclast differentiation from human peripheral blood monocytes and monocyte-derived dendritic cells. A stimulation with CX3CL1 significantly promoted osteoclast differentiation from CD16-monocytes and also monocyte-derived dendritic cells induced by macrophage colony-stimulating factor (M-CSF) and receptor activator of NF-κB ligand (RANKL). On the other hand, CD16+monocytes treated with M-CSF and RANKL did not differentiate into osteoclasts, even with CX3CL1. Calcium resorption was significantly increased by monocyte-derived osteoclasts, but not by dendritic cell-derived osteoclasts, following the addition of CX3CL1. The present results suggest that CX3CL1 directly regulates osteoclast differentiation. CX3CL1 may play important roles in the pathogenesis of RA, not only through the accumulation of inflammatory cells, but also through osteoclastogenesis.