Corticosteroids, aurothioglucose and soybean trypsin inhibitor do not prevent pemphigus antibody-induced acantholysis in vitro.
Hydrocortisone, triamcinolone acetonide, aurothioglucose and soybean trypsin inhibitor were added to normal human skin explants cultured with IgG from pemphigus serum to determine if acantholysis could be prevented. At the therapeutic concentrations used none of these compounds prevented binding of the autoantibody to the epidermal target cells, and none prevented acantholysis. These experiments support the concepts that the pemphigus antibody alone is responsible for producing the acantholytic lesions of pemphigus, that the therapeutic effectiveness of steroids and gold salts is probably due to their ability to reduce serum autoantibody titres and that pemphigus acantholysis is probably not caused by a serine proteinase.
D000051:Acantholysis / Q000276:immunology / Q000517:prevention & control; D006051:Aurothioglucose / Q000494:pharmacology*; D046508:Culture Techniques; D006046:Gold / Q000494:pharmacology*; D006801:Humans; D006854:Hydrocortisone / Q000494:pharmacology*; D007074:Immunoglobulin G; D010392:Pemphigus / Q000276:immunology / Q000517:prevention & control*; D012867:Skin / Q000187:drug effects; D014222:Triamcinolone Acetonide / Q000494:pharmacology*; D014361:Trypsin Inhibitors / Q000494:pharmacology*
D007074:Immunoglobulin G; D014361:Trypsin Inhibitors; D006051:Aurothioglucose; D006046:Gold; D014222:Triamcinolone Acetonide; D006854:Hydrocortisone