Interstitial lung disease progression in patients with anti-aminoacyl transfer-RNA-synthetase autoantibodies is characterized by higher levels of sCD163

• Patients with anti-tRNA autoantibodies with lung disease progression had higher levels of sCD163 at follow-up than patients with improvement of lung disease. • Treatment with a combination of prednisone with methotrexate and leflunomide induced stability or improvement in pulmonary function tests in 87.5% of the cohort patients . • Serum TGF-β1 levels increased independently of ILD progression in patients with ASSD. Patients with anti-tRNA autoantibodies are characterized by arthritis, mechanic´s hands, fever, Raynaud´s phenomenon, and interstitial lung disease (ILD), in at least two clinical scenarios: the antisynthetase syndrome (ASSD) and interstitial pneumonia with autoimmune features (IPAF). The anti-tRNA-ILD treatment is centered on the administration of corticosteroids and a wide variety of immunosuppressive drugs; however, the effectiveness of the treatment depends on factors not fully understood. This research work aimed to quantify the serum levels of two molecules related to pulmonary fibrosis and explore their relationship with the progression of ILD associated with ASSD Serum levels of sCD163 and TGF-β1 from baseline and after six months of treatment of ILD patients’ positives to anti-tRNA were included in the current study. At six months, patients were classified as with or without ILD progression Forty patients were included (anti-Jo1, anti-PL7, anti-PL12, and anti-Ej). Five patients (12.5%) had ILD progression and were characterized by higher levels of sCD163 at baseline. Baseline sCD163 serum levels showed good discriminatory capacity in patients with ILD progression. On the other hand, at follow-up, serum TGF-β1 levels significantly increased in both patients’ groups, with and without progression Basal levels of sCD163 were higher in patients who later developed ILD progression and kinetics of both molecules suggests the participation of M2 macrophages in the development of ILD.