Environmental and genetic predisposition have been described in interstitial lung disease associated with rheumatoid arthritis (ILD-RA), in addition to proteins that suggest different pathophysiological mechanisms of lung fibrosis. Some proteins are gelsolin (in fibrosis); SP-A protein (in inflammation) and GST, show a difference between inflammatory and fibrotic patterns in ILD-RA. Identifying protein profiles for ILD-RA will assist in improving diagnosis and prognosis in pacients; therefore, the hypothesis is that the protein profile in ILD-RA with inflammatory characteristics differs from that with fibrotic. This is a cross-sectional study, including patients with ILD-RA from the Instituto Nacional de Enfermedades Respiratorias, Mexico; the determination of a multiplex panel (11 cytokines) was carried out, in addition to PAD2, PAD4, and TGF?1 by ELISA technique, in bronchoalveolar lavage (BAL) and serum samples. Differences in serum protein levels were identified in the intra-group analysis: 4 increased proteins in the ILD-RA fibrosis compared to the inflammation (IL4, IL5, IL12-p70, IL18 and PAD4, p<0.05). In the Spearman correlation analysis of the BAL levels with clinical, spirometry, and biochemical variables, was identified: DAS28 with IL18, IL2, and PAD4; the lymphocytes in BAL with PAD4 (rho>0.5, p<0.05). Proteins associated with the extension of lung damage were identified, fibrosis 7 proteins, and ground-glass opacities with 5 proteins. In conclusion, ILD-RA with predominantly inflammatory and fibrotic phenotypes have differential proteins that provide susceptibility to a fibrosis phenotype and activity disease.