Background/Purpose: Anti-Jo-1 is an autoantibody that is specifically detected in the blood sera of patients with polymyositis/dermatomyositis (PM/DM). The corresponding antigen is known to be histidyl-tRNA synthase, an aminoacyl-tRNA synthase (ARS) localized to the cytoplasm. Recently, autoantibodies to other ARSs have been identified and patients with these antibodies have distinguishing clinical symptoms such as lesions of the lung or skin, a condition known as anti-ARS antibody syndrome. We measured anti-ARS antibodies in rheumatoid arthritis (RA) patients and evaluated its clinical characteristics.

Methods: At our hospital, 228 ambulatory RA patients were selected for the study. We evaluated the positive rate of anti-ARS antibodies in the blood sera of these patients. Anti-ARS antibodies were measured using the EUROLINE Myositis Profile 3 test system (EUROIMMUN Inc., Lubeck, Germany). Five anti-ARS antibodies can be measured using this kit: anti-OJ, anti-EJ, anti-PL-12, anti-PL-7, and anti-Jo-1 antibodies. For blood serum testing positive for any one of these antibodies, we performed an indirect immunofluorescence assay by using HEp-2 cells to determine whether a reaction occurred in the cytoplasm. We grouped the participants into anti-ARS antibody-positive and -negative groups, and evaluated age, gender , male-to-female ratio, anti-CCP antibodies, rheumatoid factor levels, presence of interstitial pneumonia (IP), and frequency of usage of methotrexate or biologics.

Results: Anti-ARS antibodies were detected in 6.1% (14 patients) of all RA patients. Specifically, anti-PL-7 antibodies were detected in 6 patients (2.6%), anti-EJ antibodies in 4 patients (1.8%), anti-PL-12 antibodies in 2 patients (0.9%), anti-OJ antibodies in 1 patient (0.4%), and anti-Jo-1 antibodies in 1 patient (0.4%). When the blood sera of these patients were allowed to react with HEp-2 cells by using the indirect immunofluorescence method, we detected staining in the cytoplasm of all patients. When we compared the anti-ARS antibody-positive and -negative groups, differences in age or gender were not observed. However, the frequency of interstitial pneumonia in the anti-ARS antibody-positive group was significantly higher (P < 0.05). A detailed investigation of the antibodies revealed that anti-PL-7 and anti-PL-12 antibodies were detected at a significantly higher level in patients with IP. Biologics were administered in 3 patients in the anti-ARS antibody-positive group; however, concomitant myositis or exacerbation of IP was not observed. No significant difference was observed between the positive and negative groups  in terms of anti-CCP antibody values or rheumatoid factor levels.

Conclusion: Anti-ARS is an autoantibody that is detected specifically in PM/DM patients; however, we demonstrated that it is also detected in RA patients. In particular, anti-PL-7 and anti-PL-12 antibodies were detected efficiently in RA patients with IP, suggesting that these autoantibodies are associated with IP. Our investigation showed that biologics could be administered safely to RA patients with anti-ARS antibodies.

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ACR Meeting Abstracts - https://acrabstracts.org/abstract/clinical-evaluation-of-anti-aminoacyl-trna-synthase-antibodies-in-rheumatoid-arthritis-patients/