No Evidence of Apoptotic Cells in Pemphigus Acantholysis
نویسندگان
چکیده
منابع مشابه
Pemphigus vulgaris acantholysis ameliorated by cholinergic agonists.
BACKGROUND Pemphigus vulgaris (PV) is an autoimmune, IgG autoantibody-mediated disease of skin and mucosa leading to progressive blistering and nonhealing erosions. Patients develop autoantibodies to adhesion molecules mediating intercellular adhesion and to keratinocyte cholinergic receptors regulating cell adhesion. OBSERVATIONS To determine whether a cholinergic agonist can abolish PV IgG-...
متن کاملScanning electron microscopy of acantholysis in pemphigus foliaceus*
We performed scanning electron microscopy of an inverted blister roof in a case of pemphigus foliaceus. The loss of intercellular adherence could be easily seen with low magnification. The acantholytic keratinocytes displayed an irregular and sometimes polygonal contour. Round cells, typically seen in light microscopy, were also observed. The examination of a blister roof allows ultrastructural...
متن کاملApoptosis is not required for acantholysis in pemphigus vulgaris.
The autoimmune blistering skin disease pemphigus vulgaris (PV) is caused primarily by autoantibodies against desmosomal cadherins. It was reported that apoptosis can be detected in pemphigus skin lesions and that apoptosis can be induced by PV-IgG in cultured keratinocytes. However, the role of apoptosis in PV pathogenesis is unclear at present. In this study, we provide evidence that apoptosis...
متن کاملApoptotic Pathways in Pemphigus
Pemphigus is a group of human autoimmune blistering diseases of the skin in which autoantibodies to desmosome cadherins induce loss of cell-cell adhesion (acantholysis). In addition to steric hindrance and activation of intracellular signaling, apoptosis has been suggested to contribute to the mechanism by which pathogenic IgG induces acantholysis. We review the current literature examining the...
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ژورنال
عنوان ژورنال: Journal of Investigative Dermatology
سال: 2014
ISSN: 0022-202X
DOI: 10.1038/jid.2014.60