Fibroblast-like synoviocytes: key effector cells in rheumatoid arthritis
By B. Bartok, Gary S. Firestein. Immunological Reviews, 2010
1,853 citations recorded by the source corpus.
Summary: 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.
Subfields: Hematology, Immunology, Rheumatology
View Paper: https://www.semanticscholar.org/paper/28f585a18c4ba32726a139af3d69b25906eab0f9
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In Rheumatology
Citations in the corpus
- Management of Rheumatoid Arthritis: An Overview (2021, background): “By comparing FLS from healthy individuals to FLS-RA it has been demonstrated that statistically significant differences can occur in heat-shock protein family A members, matrix metalloproteinase 1 (MMP1), matrix metalloproteinase 13 (MMP13) and tumor necrosis factor ligand superfamily member 10 (TNF”
- Update on the Pathomechanism, Diagnosis, and Treatment Options for Rheumatoid Arthritis (2020, background): “Moreover, the inflammatory processes in the joints of RA patients are often paralleled by neovascularization (growth of new blood vessels) and synoviocyte hyperplasia (excessive proliferation of synoviocytes) [121,122].”