| First Author | In S | Year | 1990 |
| Journal | J Clin Lab Immunol | Volume | 32 |
| Issue | 2 | Pages | 85-90 |
| PubMed ID | 1967044 | Mgi Jnum | J:12207 |
| Mgi Id | MGI:60457 | Citation | In S, et al. (1990) Treatment of end stage MRL-1pr/lpr mouse lupus disease by a cyclophosphazene derived drug and by cyclosporin A. J Clin Lab Immunol 32(2):85-90 |
| abstractText | 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. |
