Treatment of end stage MRL-1pr/lpr mouse lupus disease by a cyclophosphazene derived drug and by cyclosporin A.

Abstract

MRL-lpr/lpr mice develop T cell lymphadenopathy, polyclonal activation of B lymphocytes, autoantibodies and lupus nephritis. B and T cell populations, the dysfunctions of which play a role in the pathophysiology of the mouse disease, represent potential targets for lupus treatment. MRL-lpr/lpr mice are treated from the age of 19 weeks, i.e. after the onset of renal disease and lymphoproliferation, with Cyclosporin A which acts at the T cell level, or with DIAM4 which can down modulate polyclonal activation of B lymphocytes. DIAM4 induces the disappearance of the lymphoproliferation, the increase in C3 levels and the decrease in anti-DNA antibody, immunoglobulin and urea levels, and proteinuria. Cyclosporin A reduces lymph node hyperplasia, but has no effect on other parameters of the disease.

• Authors: S In, M Dueymes, S Appolinaire-Pilipenko, F Sournies, J F Labarre, G J Fournié
• Journal: Journal of clinical & laboratory immunology (J Clin Lab Immunol) Vol. 32 Issue 2 Pg. 85-90 (Jun 1990) ISSN: 0141-2760 [Print] Scotland
• PMID: 1967044 (Publication Type: Comparative Study, Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Aziridines
• Immunoglobulins
• Immunosuppressive Agents
• Organophosphorus Compounds
• Sodium Chloride
• Cyclosporine
• DIAM 4

Topics

• Age Factors
• Albuminuria (drug therapy, etiology)
• Animals
• Antibody Formation (drug effects)
• Aziridines (pharmacology, therapeutic use)
• Cyclosporine (pharmacology, therapeutic use)
• Hypergammaglobulinemia (drug therapy, genetics)
• Immunoglobulins (analysis)
• Immunosuppressive Agents (pharmacology, therapeutic use)
• Lupus Nephritis (complications, drug therapy, genetics)
• Lymphoproliferative Disorders (drug therapy, genetics)
• Mice
• Mice, Mutant Strains (immunology)
• Organophosphorus Compounds (pharmacology, therapeutic use)
• Sodium Chloride (pharmacology)
• Structure-Activity Relationship