SLAMF7-expressing B cells as crucial mediators in the pathogenesis of rheumatoid arthritis-interstitial lung disease

The regulatory factors involved in rheumatoid arthritis (RA) complicated with interstitial lung disease (ILD) (RAILD) remain unknown. Due to the cross-sectional nature of our study, our aim was to explore the role of the signalling lymphocytic activation molecule family (SLAMF) in RA-ILD by analysing synovial and lung samples from the Gene Expression Omnibus, animal models, and clinical samples.We collected peripheral blood mononuclear cells from patients for flow cytometry analysis of B cells, SLAMF1 protein, and SLAMF7 protein. The dataset analysis indicated a marked upregulation of SLAMF1 and SLAMF7 expression in RA synovial tissues and RA-ILD lung tissues. The same expression trend was further validated in a collagen-induced arthritis-ILD model. This suggests that B cells expressing SLAMF1 and SLAMF7 may contribute significantly to the development of lung fibrosis. Flow cytometry analysis demonstrated that SLAMF7 expression in B cells was substantially higher in RA-ILD patients than in those with RA alone. Similarly, SLAMF7 proteins were highly expressed in the plasma of patients with RA-ILD. These results suggest that SLAMF7 could be pivotal in the development and progression of RA-ILD.