Expression of Selected Integrins and Selectins in Bullous Pemphigoid

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Expression of Selected Integrins and Selectins in Bullous Pemphigoid

Blister development in bullous pemphigoid (BP) results from destruction of hemidesmosomes and basement membrane components within the dermoepidermal junction by autoantibodies. Adhesion molecules can take part in pathogenesis of this disease. The aim of the study was to determine the localization and expression of L- and E-selectins and beta1, beta3, and beta4 integrins by immunohistochemistry ...

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Differential roles for beta2 integrins in experimental autoimmune bullous pemphigoid.

Bullous pemphigoid (BP) is an autoimmune disease associated with autoantibodies directed against the hemidesmosomal antigens anti-BP230 and anti-B180. Neonatal mice injected with rabbit anti-mouse BP180 (mBP10) IgG develop a BP-like disease. Complement, immune complexes, mast cells, and neutrophils play a key role in subepidermal blistering in this animal model. In this study we investigated th...

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Expression of selected neuropeptides in pathogenesis of bullous pemphigoid and dermatitis herpetiformis.

Bullous pemphigoid (BP) and dermatitis herpetiformis (DH) are chronic subepidermal bullous diseases, which progress together with an itch and an inflammatory reaction. These symptoms may be the cause of a phenomenon described in the literature as a neurogenic skin inflammation. Neuropeptides are one of the mediators which take part in this process. The aim of our study was to indicate the expre...

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Expression of selected adhesion molecules in dermatitis herpetiformis and bullous pemphigoid.

Dermatitis herpetiformis (DH) and bullous pemphigoid (BP) are autoimmune diseases characterized by destruction of the basement membrane zone (BMZ) and anchoring fibres by autoantibodies and infiltration. Adhesion molecules can take part in these phenomena. Skin biopsies were taken from 13 patients with DH, 21 with BP, and from 10 healthy subjects. The localization and expression of E and L sele...

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ژورنال

عنوان ژورنال: Mediators of Inflammation

سال: 2007

ISSN: 0962-9351,1466-1861

DOI: 10.1155/2007/31051