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Circulating levels of mannan-binding lectin (MBL) and MBL-associated serine protease 2 in endemic pemphigus foliaceus.
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Endemic pemphigus foliaceus (EPF) is an autoimmune disease, which occurs in Brazil and other regions of South America. Mannose-binding lectin (MBL) and MBL-associated serine protease (MASP-2) play a key role in innate immunity, and its deficiency has been related to increased susceptibility to
Protease inhibitors prevent plasminogen-mediated, but not pemphigus vulgaris-induced, acantholysis in human epidermis.
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Pemphigus is an autoimmune blistering disease of the skin and mucous membranes. It is caused by autoantibodies directed against desmosomes, which are the principal adhesion structures between epidermal keratinocytes. Binding of autoantibodies leads to the destruction of desmosomes resulting in the
Effects of steroid, retinoid, and protease inhibitors on the formation of acantholysis induced in organ culture of skins from patients with benign familial chronic pemphigus.
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Skin explants from two lesional areas and four normal-appearing areas of four patients with benign familial chronic pemphigus (BFCP) were organ cultured with and without various reagents. After 24-h culturing of involved skin with medium only, dissociation of keratinocytes, which was also observed
The protease inhibitor alpha-2-macroglobulin-like-1 is the p170 antigen recognized by paraneoplastic pemphigus autoantibodies in human.
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BACKGROUND
Paraneoplastic pemphigus (PNP) is a devastating autoimmune blistering disease, involving mucocutaneous and internal organs, and associated with underlying neoplasms. PNP is characterized by the production of autoantibodies targeting proteins of the plakin and cadherin families involved in
Cytotoxic proteases in blister fluid of pemphigus and pemphigoid patients.
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Investigation of blister fluid (BF) from 49 pemphigus vulgaris and 27 bullous pemphigoid patients revealed direct interrelation between proteolytic and cytotoxic activities of BF. Human epidermal keratinocytes proved to be more sensitive to the cytolytic effect of BF as compared to human
Targeted disruption of the pemphigus vulgaris antigen (desmoglein 3) gene in mice causes loss of keratinocyte cell adhesion with a phenotype similar to pemphigus vulgaris.
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In patients with pemphigus vulgaris (PV), autoantibodies against desmoglein 3 (Dsg3) cause loss of cell-cell adhesion of keratinocytes in the basal and immediate suprabasal layers of stratified squamous epithelia. The pathology, at least partially, may depend on protease release from keratinocytes,
[Immunopathogeny of pemphigus].
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This article reviews recent concepts of pathogenetic mechanisms in pemphigus. We describe the pathogenic effect of the autoantibodies, the animal model for the disease and the ultrastructural alterations which follow the antibody-antigen interaction. The role of complement and protease systems in
Pemphigus can be induced by topical phenol as well as by foods and drugs that contain phenols or thiols.
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Pemphigus is an autoimmune disease that results from the interaction between predisposing genetic factors and exogenous factors, the most common environmental factors being drugs and food. Topical phenol has induced pemphigus in one patient. Drugs and foods that induce pemphigus are divided into
Staphylococcal scalded skin syndrome: exfoliative toxin A (ETA) induces serine protease activity when combined with A431 cells.
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Staphylococcal scalded skin syndrome is the term used for a spectrum of primarily neonatal blistering skin diseases caused by the exfoliative toxins, ETA and ETB, of Staphylococcus aureus. Despite 25 y of research, the toxins' mechanism of action is still poorly understood, although evidence
Complement fixation by pemphigus antibody. IV. Enhanced epidermal cell detachment in the absence of human plasminogen.
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It has been reportedly previously that complement enhances pemphigus vulgaris antibody-induced epidermal cell detachment. The present studies were designed to eliminate the possibility of the human plasminogen-plasmin system contributing to the cell detachment observed in previous
Pemphigus. Skin failure mediated by autoantibodies.
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Pemphigus is a group of diseases in which autoantibodies mediate a loss of cell-to-cell adhesion, resulting in blister formation and ultimate failure of the barrier function of the skin. These autoantibodies are directed against complexes that contain polypeptides found in adhering junctions.
A possible mechanism for phenol-induced pemphigus.
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A possible mechanism for phenol-induced pemphigus lesions in genetically predisposed individuals is proposed that accounts for in vitro observations and cases of biochemical acantholysis, as well as the in vivo acantholysis in pemphigus induced by phenols. The mechanism involves the induction of
Sparking Fire Under the Skin? Answers From the Association of Complement Genes With Pemphigus Foliaceus.
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Skin blisters of pemphigus foliaceus (PF) present concomitant deposition of autoantibodies and components of the complement system (CS), whose gene polymorphisms are associated with susceptibility to different autoimmune diseases. To investigate these in PF, we evaluated 992 single-nucleotide
Appearance of "pemphigus acantholysis factor" in human skin cultured with pemphigus antibody.
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These studies deal with the mechanism of pemphigus IgG-induced epidermal acantholysis. When normal human skin was culted with defined medium containing IgG from pemphigus serum, extensive epidermal acantholysis developed and heat-labile proteolytic enzyme(s) were recovered in the culture medium. The
Mast cells in developing subepidermal bullous diseases: emphasis on tryptase, chymase and protease inhibitors.
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The possible involvement of mast cell tryptase and chymase in subepidermal bullous diseases was studied enzyme-histochemically in specimens from erythematous and vesicular skin and from non-involved skin of patients with dermatitis herpetiformis, bullous pemphigoid, erythema multiforme, infective
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