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.
D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D006051:Aurothioglucose / Q000494:pharmacology; D001402:B-Lymphocytes / Q000276:immunology*; D002738:Chloroquine / Q000494:pharmacology; D003114:Colony-Forming Units Assay; D003864:Depression, Chemical; D004305:Dose-Response Relationship, Drug; D005260:Female; D005938:Glucocorticoids / Q000494:pharmacology; D007166:Immunosuppressive Agents / Q000494:pharmacology*; D008213:Lymphocyte Activation / Q000187:drug effects*; D051379:Mice; D008810:Mice, Inbred C57BL; D011453:Prostaglandins / Q000494:pharmacology; D013154:Spleen / Q000166:cytology
D000893:Anti-Inflammatory Agents; D005938:Glucocorticoids; D007166:Immunosuppressive Agents; D011453:Prostaglandins; D006051:Aurothioglucose; D002738:Chloroquine