Nf-Κb Signaling in Rheumatoid Arthritis With Focus on Fibroblast-Like Synoviocytes Publisher



Nejatbakhsh Samimi L¹ ; Farhadi E^{1, 2} ; Tahmasebi MN³ ; Jamshidi A¹ ; Sharafat Vaziri A³ ; Mahmoudi M^{1, 2} Show Affiliations
Source: Autoimmunity Highlights Published:2020

Abstract

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. © 2020 The Author(s).