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Pathogenic autoantibodies preferentially target the non\u2010collagenous 16A domain of collagen <jats:styled-content style=\"fixed-case\">XVII<\/jats:styled-content> (also called <jats:styled-content style=\"fixed-case\">BP<\/jats:styled-content> antigen 2, <jats:styled-content style=\"fixed-case\">BPAG<\/jats:styled-content>2) present in hemidesmosomes. The pathogenic anti\u2010<jats:styled-content style=\"fixed-case\">BPAG<\/jats:styled-content>2 antibodies cause the dermal\u2013epidermal separation in neonatal and adult mice as well as in cryosections of human skin. These experimental <jats:styled-content style=\"fixed-case\">BP<\/jats:styled-content> models stress a pivotal role for neutrophils and the Fc\u03b3 receptor of immunoglobulins. Mice that have been genetically manipulated in the pathogenic domain of <jats:styled-content style=\"fixed-case\">BPAG<\/jats:styled-content>2 spontaneously develop subepidermal blistering with pruritus and eosinophilic infiltration. <jats:styled-content style=\"fixed-case\">BPAG<\/jats:styled-content>2 is physiologically and aberrantly expressed in neuronal tissue and internal malignancies, and the associations of <jats:styled-content style=\"fixed-case\">BP<\/jats:styled-content> with Parkinson's disease, stroke and internal malignancies invites new investigations into the immunological dysregulation behind the comorbidity.<\/jats:p>","DOI":"10.1111\/1346-8138.13207","type":"journal-article","created":{"date-parts":[[2015,11,25]],"date-time":"2015-11-25T11:24:18Z","timestamp":1448450658000},"page":"237-240","source":"Crossref","is-referenced-by-count":13,"title":["Bullous pemphigoid: What's 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