Immunopathogenesis of rheumatoid arthritis

By Gary S. Firestein, I. McInnes. Immunity, 2017

881 citations recorded by the source corpus.

Rheumatoid arthritis (RA) is the most common inflammatory arthropathy. The majority of evidence, derived from genetics, tissue analyses, models and clinical studies, points to an immune mediated etiology associated with stromal tissue dysregulation that together propogate chronic inflammation and articular destruction. A pre-RA phase lasting months to years, may be characterized by the presence of circulating autoantibodies, increasing concentration and range of inflammatory cytokines and chemokines and altered metabolism. Clinical disease onset comprises synovitis and systemic comorbidities affecting the vasculature, metabolism and bone. Targeted immune therapeutics, and aggressive treatment strategies have substantially improved clinical outcomes, and informed pathogenetic understanding, but no cure as yet exists. Herein we review recent data that support intriguing models of disease pathogenesis. They allude to the possibility of restoration of immunologic homeostasis and thus a state of tolerance associated with drug free remission. This target represents a bold vision for the future of RA therapeutics.

Subfields: Radiology, Nuclear Medicine and Imaging, Rheumatology

View Paper: https://www.semanticscholar.org/paper/8e869cafaa9264c51990a586b72408da245a817f

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Citations in the corpus

The Sleep-Immune Crosstalk in Health and Disease (2019, background): “The immunopathology in RA is reasonably well understood and is characterized by inappropriate production of various cytokines, in particular TNF, among several other immunological abnormalities (94, 188).”