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- W1998843997 abstract "Sir, Pemphigoid (herpes) gestationis (PG) is an autoimmune subepidermal blistering disease associated with pregnancy and characterized by linear deposition of C3 and, less frequently, of immunoglobulin (Ig)G along the dermal–epidermal junction (DEJ).1 Complement‐fixing circulating IgG autoantibodies to the DEJ in serum of PG patients are mainly directed to the 180‐kDa bullous pemphigoid antigen (BP180), a transmembrane hemidesmosomal glycoprotein.2 BP180 consists of an intracellular N‐terminal globular head, a transmembrane region, and a C‐terminal ectodomain. The extracellular domain of BP180 consists of 15 collagenous and 16 noncollagenous (NC) regions harbouring different antigenic sites recognized by autoantibodies from patients with various subepidermal blistering diseases.2 The ectodomain of BP180 may be shed from the surface of basal keratinocytes by cleavage within the NC16A domain resulting in a 120‐kDa fragment (LAD‐1) that lacks a short juxtamembranous portion of the extracellular domain of BP180 (Fig. 1).3, 4 In human skin, the cleavage of BP180 results in another antigenic fragment of 97 kDa (LABD97) that can be extracted from epidermis.5 Recent findings from our laboratory suggest that LAD‐1 and LABD97 have different N‐termini.6" @default.
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- W1998843997 date "2003-08-01" @default.
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- W1998843997 title "Pemphigoid gestationis: maternal sera recognize epitopes restricted to the N-terminal portion of the extracellular domain of BP180 not present on its shed ectodomain" @default.
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- W1998843997 doi "https://doi.org/10.1046/j.1365-2133.2003.05427.x" @default.
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