Immunofluorescence on split skin for the detection and differentiation of basement membrane zone autoantibodies

Gammon, W. Ray; Fine, Jo‐David; Forbes, M A; Briggaman, Robert A.

doi:10.1016/0190-9622(92)70161-8

Cited by 112 publications

(65 citation statements)

References 38 publications

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“…22 The use of salt-split epithelial substrates most likely enhances binding of BP autoantibodies to the extracellular domain of BP180 because this method cleaves the basement membrane in the middle of the lamina lucida. 12 Furthermore, in both humans and dogs, salt-split skin indirect IF allows easy differentiation of BP from other dermatoses that target antigens located in the lower epidermal basement membrane. 12,22,29 Because many autoimmune subepidermal blistering diseases exhibit similar phenotypes, histologic lesions, and IF findings, final nosology cannot be achieved without identification of the specific antigens targeted by circulating autoantibodies.…”

Section: Discussionmentioning

confidence: 99%

“…12 Furthermore, in both humans and dogs, salt-split skin indirect IF allows easy differentiation of BP from other dermatoses that target antigens located in the lower epidermal basement membrane. 12,22,29 Because many autoimmune subepidermal blistering diseases exhibit similar phenotypes, histologic lesions, and IF findings, final nosology cannot be achieved without identification of the specific antigens targeted by circulating autoantibodies. Immunoblotting using proteins isolated from various epithelial and dermal extracts permits initial determination of the molecular mass of targeted antigen(s).…”

Section: Discussionmentioning

confidence: 99%

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Novel Feline Autoimmune Blistering Disease Resembling Bullous Pemphigoid in Humans: IgG Autoantibodies Target the NC16A Ectodomain of Type XVII Collagen (BP180/BPAG2)

Olivry

Chan

et al. 1999

Vet Pathol

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Abstract. In humans and dogs, bullous pemphigoid (BP) is an autoimmune blistering disease associated with the production of basement membrane autoantibodies that target the 180-kd type XVII collagen (BP180, BPAG2) and/or the 230-kd plakin epidermal isoform BPAG1e (BP230). In two adult cats, an acquired dermatosis and stomatitis was diagnosed as BP subsequent to the fulfillment of the following criteria: 1) presence of cutaneous vesicles, erosions, and ulcers; 2) histologic demonstration of subepidermal vesiculation with inflammatory cells, including eosinophils; 3) in vivo deposition of IgG autoantibodies at the epidermal basement membrane zone; and 4) serum IgG autoantibodies targeting a 180-kd epidermal protein identified as type XVII collagen. In both cats, the antigenic epitopes targeted by IgG autoantibodies were shown to be situated in the NC16A ectodomain of type XVII collagen, a situation similar to that of humans and dogs with BP. Feline BP therefore can be considered a clinical, histopathologic, and immunologic homologue of BP in humans and dogs.Key words: Autoimmunity; BP180; BPAG2; cats; collagen XVII; epidermal basement membrane; pemphigoid; skin.In humans, the binding of autoantibodies to glycoproteins located in the epidermal basement membrane zone often results in cutaneous blistering. 23 Based on immunochemical and molecular characterization of targeted autoantigens, the nosology of human vesicobullous diseases currently is being revised. The denomination of bullous pemphigoid (BP) presently is restricted to those blistering dermatoses characterized by inflammatory skin blisters, microscopical neutrophil-and eosinophil-rich subepidermal vesicles, and autoantibodies that target one or both BP antigens. These antigens consist of the following hemidesmosomal proteins: a 230-kd plakin epidermal isoform (BPAG1e, BP230) and/or the 180-kd transmembrane type XVII collagen (BPAG2, BP180). 3 BP is the most common autoimmune subepidermal bullous dermatosis of humans; it is the diagnosis achieved in ϳ70% of patients exhibiting antibasement membrane autoantibodies. 5 Since 1976, anecdotal cases of dogs with blistering and erosive diseases associated with basement membrane-specific autoantibodies have been reported under the umbrella diagnosis of BP. 2,4,[9][10][11]14,15,20,28,[31][32][33][35][36][37] In these cases, the specific antigen(s) targeted by autoantibodies, however, was not determined. In 1995, the canine homologue of human BP was established with the demonstration of anti-BP180 autoimmunity in a dog with cutaneous vesicles. 17 The immunologic identity of canine and human BP was further strengthened with the recent demonstration that in both species circulating IgG autoantibodies target similar antigenic epitopes in the NC16A ectodomain of type XVII collagen (BP180). 7 However, during the last 20 years, feline cases of blistering dermatoses associated with antibasement membrane autoantibodies have not been reported.The purpose of the present study was to demonstrate the existence of the feline coun...

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Novel Feline Autoimmune Blistering Disease Resembling Bullous Pemphigoid in Humans: IgG Autoantibodies Target the NC16A Ectodomain of Type XVII Collagen (BP180/BPAG2)

Olivry

Chan

et al. 1999

Vet Pathol

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“…microscopy. 72,75,76 Tissue-bound and circulating antibodies in EBA patients mainly belong to the IgG1 and IgG4 subclasses. [77][78][79][80] Wozniak and…”

Section: Immunofluorescence Studiesmentioning

confidence: 99%

Epidermolysis bullosa acquisita: What’s new?

Ishii

Hamada

Dainichi

et al. 2010

The Journal of Dermatology

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Type VII collagen is an adhesion molecule of the extracellular matrix in epithelial basement membranes, and the main constituent of anchoring fibrils at the dermal-epidermal junction (DEJ). Autoimmunity against this protein is causing the rare organ-specific epidermolysis bullosa acquisita (EBA). EBA is a rare acquired, heterogeneous, chronic blistering disease of skin disease of skin and mucous membranes characterized by subepidermal blisters and tissue-bound as well as circulating autoantibodies to the DEJ. EBA has several distinct clinical presentations with other subepidermal bullous diseases, such as mainly dystrophic epidermolysis bullosa or bullous pemphigoid. The circulating immunoglobulin G autoantibodies for EBA react with a 290-kDa dermal protein, type VII collagen, as detected by immunoblot analysis using dermal extracts. The pathogenicity of these autoantibodies has been demonstrated by experimental animal models, in which anti-type VII collagen antibodies injected into a mouse produced an EBA-like blistering disease in the animal. EBA cases often require high doses of systemic corticosteroids and a variety of immunosuppressants. Although treatment for EBA is frequently difficult and unsatisfactory, some therapeutic success has been reported with colchicine, dapsone, infliximab and i.v. immunoglobulin. In this review, we will focus on recent progress in our understanding of the clinical manifestations, the etiopathogenesis as well as the management of EBA.

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“…However, using a special indirect complement fixation immunofluorescence technique, the majority of patients' sera demonstrate complement-fixing IgG directed against an antigen of the dermal -epidermal junction, the so-called herpes gestationis factor 19,20 . If 1 M NaCl-split human skin is used as a substrate, PG autoantibodies bind to the epidermal side of the artificial blister 21 (Fig. 2).…”

Section: Immunopathology and Diagnosismentioning

confidence: 99%

Pemphigoid gestationis: new insights into the pathogenesis lead to novel diagnostic tools

Shimanovich

2002

BJOG: An International Journal of Obstetrics and Gynaecology

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Immunofluorescence on split skin for the detection and differentiation of basement membrane zone autoantibodies

Cited by 112 publications

References 38 publications

Novel Feline Autoimmune Blistering Disease Resembling Bullous Pemphigoid in Humans: IgG Autoantibodies Target the NC16A Ectodomain of Type XVII Collagen (BP180/BPAG2)

Novel Feline Autoimmune Blistering Disease Resembling Bullous Pemphigoid in Humans: IgG Autoantibodies Target the NC16A Ectodomain of Type XVII Collagen (BP180/BPAG2)

Epidermolysis bullosa acquisita: What’s new?

Pemphigoid gestationis: new insights into the pathogenesis lead to novel diagnostic tools

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