Journal
IMMUNOLOGICAL REVIEWS
Volume 233, Issue -, Pages 233-255Publisher
WILEY
DOI: 10.1111/j.0105-2896.2009.00859.x
Keywords
cytokines; rheumatoid arthritis; signaling protein; inflammation
Categories
Funding
- NIAID NIH HHS [R01 AI070555, R01 AI067752-04, R01 AI070555-04, R01 AI067752] Funding Source: Medline
- NIAMS NIH HHS [R01 AR047825, R01 AR045347-09, R01 AR047825-07, R01 AR045347] Funding Source: Medline
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI070555, R01AI067752] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES [R01AR045347, R01AR047825] Funding Source: NIH RePORTER
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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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