The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Immunopathology of bullous pemphigoid, an autoimmune and inflammatory skin blistering disease.

Bullous pemphigoid (BP) was first described by Lever in 1953 as a subepidermal blistering disease. Key immunohistological features of BP include dermo-epidermal junction (DEJ) separation, an inflammatory cell infiltrate in the upper dermis, and autoantibodies directed against two emidesmosomal antigens, BP230 and BP180. In 1993, an IgG passive transfer mouse model of BP was developed by administering rabbit anti-murine BP180 antibodies to neonatal mice. This model recapitulates the key features of human BP. Systematic dissection of this BP model has revealed that subepidermal blistering is initiated by anti-BP180 antibodies and mediated by complement activation, mast cell degranulation, and neutrophil infiltration. Proteinases and reactive oxygen species released by infiltrating neutrophils work together to damage the basement membrane zone (BMZ), causing a subepidermal blister. Recently, another novel mouse model for BP has been developed by active immunization. C57BL/6J mice actively immunized with murine BP180 develop BP-like skin lesions. The IgG passive transfer and active models of BP provide us with invaluable in vivo systems not only for dissecting cellular and humoral responses in BP but also for developing effective therapies for this disease.[1]


WikiGenes - Universities