Immunoglobulin G deposition to nonhemidesmosomal lamina lucida and early neutrophil involvement are characteristic features in a case of anti‐p200 pemphigoid. (20th November 2012)

• Record Type: Journal Article
• Authors: Shimizu, A.; Funakoshi, T.; Ishibashi, M.; Yoshida, T.; Koga, H.; Hashimoto, T.; Amagai, M.; Ishiko, A.
• Is Part Of: British journal of dermatology. Volume 168:Number 3(2013:Mar.)
• Page Start: 647
• Page End: 655
• Publication Date: 2012-11-20
• Subjects: Dermatology -- Periodicals; Skin -- Diseases -- Periodicals; 616.5
• DOI: 10.1111/bjd.12033
• Languages: English
• ISSNs: 0007-0963

Abstract

<abstract abstract-type="main" xml:lang="en"> <title>Summary</title> <p>The ultrastructural characteristics and immunolocalization of <italic>in vivo</italic> bound immunoglobulin G (IgG) in skin affected by anti‐p200 pemphigoid have not been elucidated. To give insight into the mechanism of blister formation we report a new case of anti‐p200 pemphigoid, studied with stage‐oriented morphological analysis and immunoelectron microscopy. Skin biopsy specimens were evaluated ultrastructurally and histologically with immunohistochemistry. By observing the nonblister site, the blister edge and centre of the blister, we determined that neutrophil infiltration increases gradually at the dermoepidermal junction in association with the destruction of type IV collagen. Ultrastructurally, many neutrophils were observed under the lamina densa, with vacuole formation in the dermis. At the periphery of the blister, the lamina densa became fragmented and was observed either at the roof or the floor of the blister. At the centre of the blister, the lamina densa was mainly observed at the blister floor. Postembedding immunoelectron microscopy demonstrated that the IgG, bound <italic>in vivo</italic>, localized at the lamina lucida, while the area beneath the hemidesmosomes was spared. Together with the early involvement of neutrophils and the destruction of the basal lamina, we suggest that the binding of autoantibodies to the nonhemidesmosomal lamina lucida may induce inflammation with neutrophils, resulting in blister formation.</p> </abstract>