A novel bullous pemphigoid antigen (BP125) located in the deeper layers of the basement membrane zone

Gao, S. Q.

doi:10.1001/archderm.130.7.873

Cited by 9 publications

(2 citation statements)

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“…Indirect IF microscopy on salt-split skin demonstrates, as in our patient, circulating autoantibodies binding to the dermal side of the test substrate. This binding pattern is also characteristic for antibodies that are directed to laminins 5 and 6, 17,19,26 the 105 kDa lower lamina lucida protein (p105), 21 the 125 kDa protein recognized by some BP sera, 22 and type VII collagen. 27 On immunoblotting of epidermal extracts, the serum of our patient, like that of other cases with antibodies to the 200-kDa protein, was negative.…”

Section: Discussionmentioning

confidence: 87%

Autoantibodies in anti‐p200 pemphigoid stain skin lacking laminin 5 and type VII collagen

Zillikens

Ishiko

Jonkman

et al. 2000

British Journal of Dermatology

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We report the case of a patient with a widespread bullous skin disease and linear deposits of IgG and C3 at the dermal-epidermal junction using direct immunofluorescence microscopy. Indirect immunofluorescence analysis demonstrated circulating IgG autoantibodies that stained, like autoantibodies to laminin 5 and type VII collagen, the dermal side of 1 mol L-1 NaCl-split human skin. By immunoblotting dermal extracts, the patient's serum, like serum samples from two control patients, reacted with a 200-kDa protein. Using immunoelectron microscopy, the serum labelled a component of the lower lamina lucida, but not the lamina densa/sublamina densa region, distinguishing this from the type VII collagen localization pattern. By immunofluorescence microscopy on skin sections from patients lacking either laminin 5 (Herlitz's epidermolysis bullosa) or type VII collagen (recessive dystrophic epidermolysis bullosa of Hallopeau-Siemens), the patient's serum retained reactivity with these test substrates. The patient's disease responded rapidly to the use of topical corticosteroids and lesions healed without scarring or milia formation. Our results provide strong evidence for the hypothesis that the 200 kDa autoantigen is different from laminin 5 and type VII collagen. For this new disease, we propose the designation 'anti-p200 pemphigoid'.

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Section: Discussionmentioning

confidence: 87%

Autoantibodies in anti‐p200 pemphigoid stain skin lacking laminin 5 and type VII collagen

Zillikens

Ishiko

Jonkman

et al. 2000

British Journal of Dermatology

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“…Thus, our patient’s results of indirect IF using skin split with 1 M NaCl and immunoblot analysis differed from those of BP and LABD. In addition, a 105-kD antigen has been reported as a novel antigen of some subepidermal blistering dermatosis resembling clinically severe toxic epidermal necrolysis [9], and a novel 125-kD antigen in a patient with clinical features of BP has also been reported [10]. Those two antigens were shown to locate to the dermal side of the split skin.…”

Section: Discussionmentioning

confidence: 99%

A Case of Unique Subepidermal Blistering Disease with Autoantibodies against a Novel Dermal 200-kD Antigen

Kawahara

Matsuo²,

Hashimoto³

et al. 1998

Dermatology

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Background: Several autoimmune subepidermal blistering diseases with autoantibodies against the epidermal basement membrane zone (BMZ) have been identified. Each shows distinct immunological findings. Objectives: Our patient showed clinical features which were indicative of bullous pemphigoid or linear IgA bullous dermatosis. In his serum, circulating IgG antibodies binding to the dermal side of skin split with 1 M NaCl were detected. To clarify the immunological character of the patient, we performed further studies. Methods: Western immunoblot analysis using normal human skin extracts and indirect immunofluorescence (IF) with affinity-purified IgG antibodies to the detected dermal protein were done. Results: Western immunoblot analysis demonstrated IgG antibodies reacting with a dermal 200-kD protein. Affinity-purified IgG antibodies to the 200-kD protein reacted to the dermal side of the split by indirect IF. Therefore, this dermal 200-kD protein is believed to be the epidermal BMZ antigen. Conclusion: Our patient showed an immunologically unique subepidermal blistering disease.

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Basement membrane zone

Ray

Gately

1996

Clinics in Dermatology

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A novel bullous pemphigoid antigen (BP125) located in the deeper layers of the basement membrane zone

Cited by 9 publications

References 0 publications

Autoantibodies in anti‐p200 pemphigoid stain skin lacking laminin 5 and type VII collagen

Autoantibodies in anti‐p200 pemphigoid stain skin lacking laminin 5 and type VII collagen

A Case of Unique Subepidermal Blistering Disease with Autoantibodies against a Novel Dermal 200-kD Antigen

Basement membrane zone

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