Monocytes from patients with rheumatoid arthritis release increased amount of reactive oxygen intermediates

Respiratory burst mechanisms essential for the degradation of ingested complexes could contribute to the pathogenesis of rheumatoid arthritis (RA) by causing tissue injury. Monitoring the generation of superoxide and hydrogen peroxide blood monocytes from patients with RA reveals that these monocytes on stimulation release a higher amount of reactive oxygen intermediates when compared to the release by normal macrophages. It shows that monocytes from RA patients have high oxidative burst capacity which is suggestive of an important role for these cells in the pathophysiology of RA.