Destructive Roles of Fibroblast-like Synoviocytes in Chronic Inflammation and Joint Damage in Rheumatoid Arthritis
- PMID: 33113036
- DOI: 10.1007/s10753-020-01371-1
Destructive Roles of Fibroblast-like Synoviocytes in Chronic Inflammation and Joint Damage in Rheumatoid Arthritis
Erratum in
-
Correction to: Destructive Roles of Fibroblast-Like Synoviocytes in Chronic Inflammation and Joint Damage in Rheumatoid Arthritis.Inflammation. 2021 Apr;44(2):480. doi: 10.1007/s10753-020-01402-x. Inflammation. 2021. PMID: 33319320 No abstract available.
Abstract
Fibroblast-like synoviocytes (FLSs) are important non-immune cells located mostly in the inner layer of the synovium. Indeed, these cells are specialized mesenchymal cells, implicated in collagen homeostasis of the articular joint and provide extracellular matrix (ECM) materials for cartilage and contribute to joint destruction via multiple mechanisms. RA FLS interactions with immune and non-immune cells lead to the development and organization of tertiary structures such as ectopic lymphoid-like structures (ELSs), tertiary lymphoid organs (TLOs), and secretion of proinflammatory cytokines. The interaction of RA FLS cells with immune and non-immune cells leads to stimulation and activation of effector immune cells. Pathological role of RA FLS cells has been reported for many years, while molecular and cellular mechanisms are not completely understood yet. In this review, we tried to summarize the latest findings about the role of FLS cells in ELS formation, joint destruction, interactions with immune and non-immune cells, as well as potential therapeutic options in rheumatoid arthritis (RA) treatment. Our study revealed data about interactions between RA FLS and immune/non-immune cells as well as the role of RA FLS cells in joint damage, ELS formation, and neoangiogenesis, which provide useful information for developing new approaches for RA treatment.
Keywords: Immune and non-immune cells; ectopic lymphoid-like structures (ELSs); fibroblast-like synoviocytes (FLSs); rheumatoid arthritis (RA).
References
-
- Karami J, Masoumi M, Khorramdelazad H, Bashiri H, Darvishi P, Sereshki HA et al. 2020. Role of autophagy in the pathogenesis of rheumatoid arthritis: latest evidence and therapeutic approaches. Life Sciences. 117734.
-
- Fang, Q., C. Zhou, and K.S. Nandakumar. 2020. Molecular and cellular pathways contributing to joint damage in rheumatoid arthritis. Mediators of Inflammation 2020: 1–20.
-
- McInnes, I.B., and G. Schett. 2011. The pathogenesis of rheumatoid arthritis. New England Journal of Medicine 365 (23): 2205–2219.
-
- Gregersen, P.K., J. Silver, and R.J. Winchester. 1987. The shared epitope hypothesis. An approach to understanding the molecular genetics of susceptibility to rheumatoid arthritis. Arthritis & Rheumatism: Official Journal of the American College of Rheumatology. 30 (11): 1205–1213.
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Medical
