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Elevated autoantibodies against interleukin‐17F correlate with disease activity in patients with early rheumatoid arthritis
Author(s) -
Yang Lin,
Bai Li,
Wei Feifei,
Liu Yuan,
Sun Lin,
Wang Wenming,
Liu Xiangyuan,
Wang Yongfu
Publication year - 2016
Publication title -
international journal of rheumatic diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.795
H-Index - 41
eISSN - 1756-185X
pISSN - 1756-1841
DOI - 10.1111/1756-185x.12618
Subject(s) - medicine , rheumatoid arthritis , autoantibody , immunology , disease , interleukin , autoimmune disease , arthritis , antibody , cytokine
Abstract Aim To investigate the presence of autoantibodies ( aA bs) against interleukin ( IL )‐17A and IL ‐17F and observe whether anti‐ IL ‐17A or IL ‐17F aA bs are associated with disease activity in patients with early rheumatoid arthritis ( ERA ). Methods At present, 60 patients with ERA , 72 patients with osteoarthritis ( OA ) and 61 healthy controls ( HC ) have been included in a database. Clinical assessment and laboratory data were recorded. We detected the titer of aA bs against IL ‐17A and IL ‐17F using enzyme‐linked immunosorbent assay and analyzed the correlation of these aA bs in patients with ERA. Results Our results showed that the levels of aA bs against IL ‐17A and IL ‐17F were significantly higher in ERA OA and HC ( P  < 0.0001). The level of aA bs against IL ‐17F was correlated with Disease Activity Score‐28 erythrocyte sedimentation rate ( ESR ) ( P  = 0.0457) and ESR alone ( P  =   0.0032) in patients with ERA . In addition, in the ERA group, the level of C‐reactive protein and rheumatoid factor immunoglobulin M was lower in patients with aA bs against IL ‐17F than patients without aA bs ( P  =   0.0247; P  =   0.0439). No significant correlation was observed between the clinical characteristics and level of aA bs against IL ‐17A in patients with ERA except ESR ( P  =   0.0239). Conclusions Elevated aA bs against IL ‐17F correlate with disease activity in patients with ERA . This evidence suggests that anti‐ IL ‐17F aA bs may have a protective role in the pathogenesis of ERA.

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