The pathogenic mechanisms of blister formation in bullous pemphigoid.
作者： Katsuichi Naito , Shinji Morioka , Hideoki Ogawa
DOI: 10.1111/1523-1747.EP12500082
关键词: Immunology 、 Human skin 、 Chemistry 、 Trypsin inhibitor 、 Macroglobulin 、 Pepstatin 、 In vivo 、 Antibody 、 Molecular biology 、 Bullous pemphigoid 、 Immunofluorescence
摘要: Normal human skin was cultured with sera, IgG fractions, and blister fluids (BF) from patients bullous pemphigoid. Antibody binding (IgG) observed by immunofluorescence techniques at the dermal-epidermal junction of all explants BF. Dermal-epidermal separation only in 19 out 20 BF obtained fresh bullae. In addition, can be produced vivo 6hr after injection into dorsal Hartley guinea pigs. not heat-inactivated (56°C, 30min) BF, although antibody observed. did occur when were preincubated rabbit antihuman C1, C3, C4, C5 antibodies. These observations suggested that both complement essential for production separation. Since patient sera failed to produce dermal- epidermal separation, other factor(s) present but absent serum might necessary The addition proteinase inhibitors, pepstatin, EDTA, soy bean trypsin inhibitor, inhibit formation contrast, presence α 2 -macroglobulin inhibited
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