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

Yoshiyuki Ohsugi, M. Eric Gershwin

Research output: Contribution to journalArticle

2 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)1-7
Number of pages7
JournalImmunopharmacology
Volume7
Issue number1
DOIs
StatePublished - 1984

Keywords

  • Antiarthritic drugs
  • Autoimmunity
  • B cell colony formation

ASJC Scopus subject areas

  • Pharmacology

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