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rdf:type |
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|
lifeskim:mentions |
|
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pubmed:issue |
4
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pubmed:dateCreated |
2009-3-26
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pubmed:abstractText |
Bullous pemphigoid (BP) is a prototypical organ-specific autoimmune disease. Autoantibodies unfold their blister-inducing potential by triggering an Fcgamma-dependent inflammatory reaction. The study by Iwata et al. in this issue provides the first direct evidence that IgG autoantibodies from BP patients may also weaken cell-matrix adhesion by depleting BP180/type XVII collagen from cultured keratinocytes. These novel findings shed new light on additional mechanisms of blister formation in pemphigoid diseases and open the way for further informative studies.
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pubmed:commentsCorrections |
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pubmed:language |
eng
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pubmed:journal |
|
|
pubmed:citationSubset |
IM
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|
pubmed:chemical |
|
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pubmed:status |
MEDLINE
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pubmed:month |
Apr
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pubmed:issn |
1523-1747
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pubmed:author |
|
|
pubmed:issnType |
Electronic
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pubmed:volume |
129
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
822-4
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pubmed:meshHeading |
|
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pubmed:year |
2009
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pubmed:articleTitle |
Bullous pemphigoid: a prototypical antibody-mediated organ-specific autoimmune disease.
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|
pubmed:affiliation |
Department of Dermatology, University Medical Center Freiburg, Freiburg, Germany. csitaru@fastmail.fm
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pubmed:publicationType |
Journal Article,
Comment,
Research Support, Non-U.S. Gov't
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