Abstract

Early diagnosis is critical to improve outcomes in rheumatoid arthritis (RA), but current diagnostic tools have limited sensitivity. Here we report a large-scale multicenter study involving training and validation cohorts of 3,262 participants. We show that serum levels of soluble scavenger receptor-A (sSR-A) are increased in patients with RA and correlate positively with clinical and immunological features of the disease. This discriminatory capacity of sSR-A is clinically valuable and complements the diagnosis for early stage and seronegative RA. sSR-A also has 15.97% prevalence in undifferentiated arthritis patients. Furthermore, administration of SR-A accelerates the onset of experimental arthritis in mice, whereas inhibition of SR-A ameliorates the disease pathogenesis. Together, these data identify sSR-A as a potential biomarker in diagnosis of RA, and targeting SR-A might be a therapeutic strategy.

Highlights

  • Diagnosis is critical to improve outcomes in rheumatoid arthritis (RA), but current diagnostic tools have limited sensitivity

  • We first assessed the levels of soluble scavenger receptor-A (sSR-A) in patients with RA or other types of rheumatic diseases and non-autoimmune inflammatory diseases

  • Elevation of sSR-A was previously reported in patients with hepatitis[23,24], the levels of sSR-A in RA patients were much higher compared to those in patients with autoimmune hepatitis (AIH, Fig. 1b)

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Summary

Introduction

Diagnosis is critical to improve outcomes in rheumatoid arthritis (RA), but current diagnostic tools have limited sensitivity. We show that serum levels of soluble scavenger receptor-A (sSR-A) are increased in patients with RA and correlate positively with clinical and immunological features of the disease This discriminatory capacity of sSR-A is clinically valuable and complements the diagnosis for early stage and seronegative RA. Administration of SR-A accelerates the onset of experimental arthritis in mice, whereas inhibition of SR-A ameliorates the disease pathogenesis Together, these data identify sSR-A as a potential biomarker in diagnosis of RA, and targeting SR-A might be a therapeutic strategy. We provide compelling evidence to show that increasing the levels of SR-A accelerates arthritis progression whereas inhibition of SR-A ameliorates disease severity These findings support diverse functions of SR-A under different pathological conditions, and might provide diagnostic and therapeutic strategies for clinical management of RA

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