Particulate matter (such as PM2.5) induces bronchus-associated lymphoid tissue formation in the respiratory tract, activating antigen-presenting cells such as dendritic cells and enhancing T-cell and B-cell activation; this process facilitates generation of autoantibodies—anti-citrullinated protein antibodies (ACPA) and rheumatoid factor—whose elevated serum levels may indicate a higher risk of joint destruction, and disrupts immune tolerance, becoming a crucial early event in RA pathogenesis [23]. This evidence concerns the gene PRTN3 and rheumatoid arthritis.