Monocyte-derived clastogenic factor in rheumatoid arthritis.

Blood or lymphocyte cultures from patients with rheumatoid arthritis show increased chromosome breakage. This is due to the presence of a clastogenic factor (CF) inducing also chromosome damage in blood cultures of healthy persons. CF may be isolated not only from patients' plasma or synovial fluid, but also from the supernatant of blood or lymphocyte cultures. No CF was detectable, if the lymphocyte cultures were free of other contaminating blood cells. Addition of neutrophils did not considerably influence the production of CF, and platelets were without any effect. However, addition of increasing numbers of monocytes resulted in increasing clastogenic activity. Also monocytes in adherence, in absence of lymphocytes and without any chemical stimulant, produced CF. This indicates that monocytes are responsible for CF production. The protective effect of superoxide dismutase, as well against CF formation as against CF action on cells of normal subjects, suggests a role of the superoxide radical O2-. Inhibitors of arachidonic acid metabolism were only slightly anticlastogenic.