Immunomodulatory interactions of suppressor cells, cell-mediated immunity, and cyclophosphamide in experimental pyelonephritis.
The recent observation that the administration of cyclophosphamide, an immunosuppressive agent, leads to the eradication of bacterial infection in experimental pyelonephritis seems paradoxical. However, cyclophosphamide is also an immunostimulator and, on the basis of its known characteristics, could enhance cell-mediated immunity either by modulation of suppressor cell activity or by depletion of infection-induced suppressor cells. This study examined these alternatives and the relation between suppressor cells, cell-mediated immunity, and cyclophosphamide administration. Cyclophosphamide enhanced the resistance of lymphocytes to the activity of suppressor cells but did not enhance cell-mediated immunity.
D000818:Animals; D002478:Cells, Cultured; D003520:Cyclophosphamide / Q000494:pharmacology*; D004927:Escherichia coli Infections / Q000276:immunology*; D008213:Lymphocyte Activation / Q000187:drug effects*; D008214:Lymphocytes / Q000187:drug effects / Q000276:immunology; D011704:Pyelonephritis / Q000276:immunology*; D051381:Rats; D050378:T-Lymphocytes, Regulatory / Q000276:immunology*
D003520:Cyclophosphamide