Inflammatory Cell Migration in Rheumatoid Arthritis: A Comprehensive Review.
Inflammatory Cell Migration in Rheumatoid Arthritis: A Comprehensive Review.
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类风湿关节炎中的炎症细胞迁移：全面评论。
DOI：
10.1007/s12016-015-8520-9
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发表时间：
2016-08
影响因子：
9.1
通讯作者：
Pereira JP
中科院分区：
文献类型：
--
作者：
Nevius E;Gomes AC;Pereira JP
类风湿性关节炎（RA）是一种主要影响关节的慢性炎症性自身免疫性疾病。自身反应性 B 和 T 淋巴细胞合作促进针对自身蛋白的抗体反应，是疾病的主要驱动因素。 T 淋巴细胞也独立于 B 淋巴细胞而促进 RA，主要通过产生促进病理的关键炎症细胞因子（例如 IL-17）。虽然人们对引发自身反应性适应性免疫反应的先天信号知之甚少，但该疾病主要是由关节组织中的炎症细胞浸润和积累以及骨吸收破骨细胞驱动的骨侵蚀引起的。破骨细胞是由多个骨髓细胞融合形成的巨大多核细胞，需要短程信号（例如细胞因子 MCSF 和 RANKL）才能进行分化。通过化学引诱剂将破骨细胞前体募集并定位到破骨细胞分化位点是控制破骨细胞生成和骨吸收的重要点。最近，GPCR EBI2 及其氧甾醇配体 7a、25 二羟基胆固醇被确定为破骨细胞前体靠近骨表面定位以及稳态下破骨细胞分化的重要调节因子。在 RA 等慢性炎症性疾病中，破骨细胞分化也由 TNFa 和 IL-1 等炎症细胞因子驱动，并且可以独立于 RANKL 发生。最后，越来越多的证据表明，引导破骨细胞前体到达发炎关节部位的趋化信号会导致疾病，因此引起了人们的极大兴趣。进一步了解复杂的骨免疫细胞相互作用应该为 RA 的治疗干预提供新的途径。
Rheumatoid arthritis (RA) is a chronic inflammatory autoimmune disease that primarily affects the joints. Self-reactive B and T lymphocytes cooperate to promote antibody responses against self proteins and are major drivers of disease. T lymphocytes also promote RA independently of B lymphocytes mainly through the production of key inflammatory cytokines, such as IL-17, that promote pathology. While the innate signals that initiate self-reactive adaptive immune responses are poorly understood, the disease is predominantly caused by inflammatory cellular infiltration and accumulation in articular tissues, and by bone erosions driven by bone-resorbing osteoclasts. Osteoclasts are giant multinucleated cells formed by the fusion of multiple myeloid cells that require short-range signals, such as the cytokines MCSF and RANKL, for undergoing differentiation. The recruitment and positioning of osteoclast precursors to sites of osteoclast differentiation by chemoattractants is an important point of control for osteoclastogenesis and bone resorption. Recently, the GPCR EBI2 and its oxysterol ligand 7a, 25 dihydroxycholesterol were identified as important regulators of osteoclast precursor positioning in proximity to bone surfaces, and of osteoclast differentiation under homeostasis. In chronic inflammatory diseases like RA, osteoclast differentiation is also driven by inflammatory cytokines such as TNFa and IL-1, and can occur independently of RANKL. Finally, there is growing evidence that the chemotactic signals guiding osteoclast precursors to inflamed articular sites contribute to disease and are of great interest. Furthering our understanding of the complex osteoimmune cell interactions should provide new avenues of therapeutic intervention for RA.
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DOI：
10.1084/jem.20092210
发表时间：
2010-05-10
期刊：
The Journal of experimental medicine
影响因子：
--
作者：
Allende ML;Tuymetova G;Lee BG;Bonifacino E;Wu YP;Proia RL
通讯作者：
Proia RL
影响因子：
4.9
作者：
Cavanagh LL;Boyce A;Smith L;Padmanabha J;Filgueira L;Pietschmann P;Thomas R
通讯作者：
Thomas R
DOI：
10.1084/jem.190.12.1741
发表时间：
1999-12-20
期刊：
The Journal of experimental medicine
影响因子：
--
作者：
Arai F;Miyamoto T;Ohneda O;Inada T;Sudo T;Brasel K;Miyata T;Anderson DM;Suda T
通讯作者：
Suda T
影响因子：
4.9
作者：
Adamopoulos IE;Chao CC;Geissler R;Laface D;Blumenschein W;Iwakura Y;McClanahan T;Bowman EP
通讯作者：
Bowman EP
影响因子：
--
作者：
AKAHOSHI, T;WADA, C;MATSUSHIMA, K
通讯作者：
MATSUSHIMA, K