Fibroblast-like synoviocytes: key effector cells in rheumatoid arthritis.

Fibroblast-like synoviocytes: key effector cells in rheumatoid arthritis.
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DOI:
10.1111/j.0105-2896.2009.00859.x
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发表时间:
2010-01
影响因子:
8.7
通讯作者:
Firestein GS
Firestein GS
中科院分区:
医学1区
文献类型:
--
作者:
Bartok B;Firestein GS

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风湿性关节炎(RA)仍然是一个重大的未满足的医疗需求,尽管显着的治疗进展。RA的发病机制是复杂的,包括许多细胞类型,包括T细胞、B细胞和巨噬细胞。滑膜内膜中的成纤维细胞样滑膜细胞(FLS)也通过产生使炎症持续的细胞因子和导致软骨破坏的蛋白酶发挥关键作用。风湿性关节炎FLS形成独特的侵袭性表型,其增加对细胞外基质的侵袭性并进一步加剧关节损伤。FLS生物学的最新进展,包括其调节先天免疫反应和激活控制其行为的细胞内信号传导机制,为疾病机制提供了新的见解。靶向FLS的新药物可以潜在地补充目前的疗法,而不会对适应性免疫应答产生重大有害影响。
Rheumatoid arthritis (RA) remains a significant unmet medical need despite significant therapeutic advances. The pathogenesis of RA is complex and includes many cell types, including T cells, B cells, and macrophages. Fibroblast-like synoviocytes (FLS) in the synovial intimal lining also play a key role by producing cytokines that perpetuate inflammation and proteases that contribute to cartilage destruction. Rheumatoid FLS develop a unique aggressive phenotype that increases invasiveness into the extracellular matrix and further exacerbates joint damage. Recent advances in understanding the biology of FLS, including their regulation regulate innate immune responses and activation of intracellular signaling mechanisms that control their behavior, provide novel insights into disease mechanisms. New agents that target FLS could potentially complement the current therapies without major deleterious effect on adaptive immune responses.
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