NF-κB signaling in rheumatoid arthritis with focus on fibroblast-like synoviocytes
NF-κB signaling in rheumatoid arthritis with focus on fibroblast-like synoviocytes
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DOI：
10.1186/s13317-020-00135-z
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发表时间：
2020-08-08
影响因子：
--
通讯作者：
Mahmoudi M
中科院分区：
文献类型：
--
作者：
Nejatbakhsh Samimi L;Farhadi E;Tahmasebi MN;Jamshidi A;Sharafat Vaziri A;Mahmoudi M
核因子-κB （NF-κB）信号通路调节先天和适应性免疫细胞的多个过程。该途径通过调节细胞因子、趋化因子和粘附分子表达参与炎症反应。NF-κB转录因子也参与细胞的存活、增殖和分化。因此，NF-κB激活失调参与了炎症性疾病的发病机制。类风湿关节炎（RA）是一种异质性和复杂的自身免疫性炎症性疾病。虽然不同的免疫和非免疫细胞参与RA的发病机制，但成纤维细胞样滑膜细胞（FLSs）在疾病进展中起着至关重要的作用。这些细胞在疾病期间发生改变并产生炎症介质，包括炎症细胞因子和基质金属蛋白酶，导致关节和软骨侵蚀。在不同的细胞信号通路中，NF-κB激活失调似乎与RA的炎症图像有关。NF-κB活化还能促进RA-FLS的增殖，抑制FLS凋亡导致RA滑膜增生。本文就NF-κB转录因子在免疫细胞和非免疫细胞（尤其是FLSs）中参与RA发病机制的作用进行综述。
The nuclear factor-κB (NF-κB) signaling pathway regulates multiple processes in innate and adaptive immune cells. This pathway is involved in inflammation through the regulation of cytokines, chemokines, and adhesion molecules expression. The NF-κB transcription factor also participates in the survival, proliferation, and differentiation of cells. Therefore, deregulated NF-κB activation contributes to the pathogenesis of inflammatory diseases. Rheumatoid arthritis (RA) is classified as a heterogeneous and complex autoimmune inflammatory disease. Although different immune and non-immune cells contribute to the RA pathogenesis, fibroblast-like synoviocytes (FLSs) play a crucial role in disease progression. These cells are altered during the disease and produce inflammatory mediators, including inflammatory cytokines and matrix metalloproteinases, which result in joint and cartilage erosion. Among different cell signaling pathways, it seems that deregulated NF-κB activation is associated with the inflammatory picture of RA. NF-κB activation can also promote the proliferation of RA-FLSs as well as the inhibition of FLS apoptosis that results in hyperplasia in RA synovium. In this review, the role of NF-κB transcription factor in immune and non-immune cells (especially FLSs) that are involved in RA pathogenesis are discussed.
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