ACR CONVERGENCE 2020—Rheumatoid arthritis (RA) has been postulated to develop in several phases, with inherited susceptibility factors in some cases leading to asymptomatic (or preclinical) citrullinated protein-directed autoimmunity, followed, after some interval, by the development of synovial infiltration and polyarticular disease. We know early treatment of RA is critical to reduce disease symptoms and slow disease progression. So is it possible to identify and treat at-risk patients during the preclinical phase to prevent disease onset?
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This session, moderated by Stanford University’s William Robinson, MD, PhD, and presented by Ronald F. Van Vollenhoven, MD, PhD, Amsterdam UMC; Peter Taylor, MD, PhD, MA, University of Oxford; and V. Michael Holers, MD, University of Colorado, reviewed research underway to examine pathogenic mechanisms responsible for the development of preclinical autoimmunity and subsequent overt disease. A case was made for the role of B cells in disease development and the rationale for targeting these cells in people identified at risk of RA.
Other research suggests that preclinical disease may be initiated in mucosal sites, primarily in the lung, due to molecular changes from environmental exposures such as cigarette smoke. Further research may pave the way for therapeutically targeting the mechanisms of preclinical disease.
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