Ketoconazole's inhibition of fungal antigen-induced thymidine uptake by lymphocytes from patients with psoriasis.
Ketoconazole, an oral antifungal imidazole, has been effective in some refractory cases of psoriasis, particularly those with scalp involvement, perhaps because of suppression of Pityrosporum ovale. To assess an ancillary immunologically mediated role for ketoconazole, its effects were evaluated on psoriatic patients' lymphocyte function. Ketoconazole in vitro markedly inhibited Pityrosporum antigen-induced lymphocyte blastogenesis as indicated by impairment of cellular tritiated thymidine uptake. Ketoconazole likewise inhibited lymphocyte uptake of other pyrimidine nucleosides by both normal and psoriatic lymphocytes. Neither imidazole or an investigational triazole antifungal (Bay n7133) inhibited the uptake. Thus, ketoconazole potentially could affect psoriasis in seborrheic areas of skin by a direct antifungal action or indirectly by suppressing fungal antigen-induced lymphocyte-mediated immune responses affecting the skin.
D000946:Antigens, Fungal / Q000276:immunology*; D002478:Cells, Cultured; D006801:Humans; D066298:In Vitro Techniques; D007654:Ketoconazole / Q000494:pharmacology* / Q000627:therapeutic use; D008213:Lymphocyte Activation / Q000187:drug effects*; D008214:Lymphocytes / Q000276:immunology; D008290:Malassezia / Q000187:drug effects / Q000276:immunology*; D008297:Male; D011565:Psoriasis / Q000097:blood* / Q000188:drug therapy / Q000276:immunology; D013936:Thymidine / Q000378:metabolism; D014316:Tritium
D000946:Antigens, Fungal; D014316:Tritium; D007654:Ketoconazole; D013936:Thymidine