The capability of plasma cells in inducible bronchus-associated lymphoid tissue to produce ACPA and RF [21], as well as the increased presence of airway abnormalities in arthritis-free individuals with serum RF and/or ACPA positivity as compared with ACPA- and RF-negative controls [22], may indicate a role for the respiratory system in the initiation of RA-AAB. This evidence concerns the gene PRTN3 and arthritic joint disease.