Inhibition by various antiarthritic agents of murine splenic B cell colony formation

There is accumulated evidence suggesting that a polyclonal B cell activation is a primary etiologic defect of autoimmune diseases in both mice and humans. Based on this previous finding, the influence of various antiarthritic agents on lipopolysaccharide-induced B cell colony formation in mouse spleen cells was studied. When added to cell culture, aurothioglucose, chloroquine, and prostaglandin E1 had a suppressive effect on B cell colony formation at clinically relevant concentrations. A 50% suppression was obtained at 10(-7) to 10(-8) M for aurothioglucose, 10(-7) M for chloroquine, and 10(-7) to 10(-8) M for prostaglandin E1, respectively. All of the immunosuppressive drugs and glucocorticoids examined decreased the number of colonies with a variety of intensity. Nonsteroidal antiinflammatory drugs have only a slight inhibitory effect at high concentrations. Both penicillamine and levamisole had no effect on B cell colony formation. This experimental system might be useful in searching for new and unique drugs and in evaluating the mode of action of drugs used against autoimmune diseases.