Inhibition of a Langerhans cell-mediated immune response by treatment modalities useful in psoriasis.
Neither the pathogenesis of psoriasis nor the mechanism whereby seemingly diverse therapies alter the disease is understood. In this study, several antipsoriatic agents were tested for their effects on the skin cell lymphocyte reaction (SLR), an immunologic assay in which HLA-DR antigens on Langerhans cells (LC) stimulate proliferation of allogeneic lymphocytes. Every agent tested (cortisol, methotrexate, hyperthermia, anthralin) inhibited the SLR at therapeutic dose levels. By contrast, a variety of antibiotics, an anti-inflammatory agent, and lithium carbonate and propranolol, two drugs known to be ineffective in psoriasis, failed to inhibit the SLR. Finally, we have shown that hyperthermia and anthralin treatments are toxic for LC whereas they have little or no effect on keratinocyte viability. These results suggest that antipsoriatic agents may act in psoriasis by alteration or killing of LC.
D000875:Anthralin / Q000494:pharmacology; D002470:Cell Survival / Q000187:drug effects; D000078404:Epidermal Cells; D006358:Hot Temperature / Q000627:therapeutic use; D006801:Humans; D006854:Hydrocortisone / Q000494:pharmacology; D066298:In Vitro Techniques; D007801:Langerhans Cells / Q000276:immunology*; D008727:Methotrexate / Q000494:pharmacology; D009504:Neutrophils / Q000276:immunology; D011565:Psoriasis / Q000188:drug therapy / Q000276:immunology / Q000628:therapy*
D000875:Anthralin; D006854:Hydrocortisone; D008727:Methotrexate