Immunopathogenesis of Rheumatoid Arthritis

Publication date: 21 February 2017
Source:Immunity, Volume 46, Issue 2
Author(s): Gary S. Firestein, Iain B. McInnes
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.

Teaser

Elucidation of the immune pathogenesis of rheumatoid arthritis has prompted significant therapeutic progress. Firestein and McInnes review recent advances in understanding of immune dysregulation and stromal pathology in RA that promote development and perpetuation of disease and offer exciting new therapeutic potential.


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