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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
1982-12-18
pubmed:abstractText
Normal human skin was cultured with sera, IgG fractions, and blister fluids (BF) from patients with bullous pemphigoid. Antibody binding (IgG) was observed by immunofluorescence techniques at the dermal-epidermal junction of all skin explants culture with sera, IgG fractions, and BF. Dermal-epidermal separation was observed only in the skin explants cultured with BF. Dermal-epidermal separation was observed in 19 out of 20 explants cultured with BF obtained from fresh bullae. In addition, dermal-epidermal separation can be produced in vivo 6 hr after the injection of BF into the dorsal skin of Hartley guinea pigs. Dermal-epidermal separation was not observed in skin explants cultured with heat-inactivated (56 degrees, C 30 min) BF, although antibody binding was observed. In addition, dermal-epidermal separation did not occur when the BF were preincubated with rabbit antihuman C1, C3, C4, and C5 antibodies. These observations suggested that both antibody and complement were essential for the production of dermal-epidermal separation. Since patient sera failed to produce dermal-epidermal separation, other factor(s) present in BF but absent from serum might be necessary for the production of dermal-epidermal separation. The addition of the proteinase inhibitors, pepstatin, EDTA, and soy bean trypsin inhibitor, did not inhibit the formation of dermal-epidermal separation. In contrast, the presence of alpha 2-macroglobulin inhibited dermal-epidermal separation.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0022-202X
pubmed:author
pubmed:issnType
Print
pubmed:volume
79
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
303-6
pubmed:dateRevised
2004-11-17
pubmed:meshHeading
pubmed:year
1982
pubmed:articleTitle
The pathogenic mechanisms of blister formation in bullous pemphigoid.
pubmed:publicationType
Journal Article