Immunoglobulin G deposition to nonhemidesmosomal lamina lucida and early neutrophil involvement are characteristic features in a case of anti-p200 pemphigoid

A. Shimizu, Takeru Funakoshi, M. Ishibashi, Tadashi Yoshida, H. Koga, T. Hashimoto, Masayuki Amagai, A. Ishiko

Research output: Contribution to journalArticle

6 Citations (Scopus)

Abstract

The ultrastructural characteristics and immunolocalization of in vivo 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 antip200 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 in vivo, 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.

Original languageEnglish
Pages (from-to)647-655
Number of pages9
JournalBritish Journal of Dermatology
Volume168
Issue number3
DOIs
Publication statusPublished - 2013 Mar

Fingerprint

Bullous Pemphigoid
Blister
Neutrophils
Immunoglobulin G
Immunoelectron Microscopy
Hemidesmosomes
Skin
Collagen Type IV
Neutrophil Infiltration
Dermis
Vacuoles
Basement Membrane
Autoantibodies
Immunohistochemistry
Inflammation
Biopsy

ASJC Scopus subject areas

  • Dermatology
  • Medicine(all)

Cite this

Immunoglobulin G deposition to nonhemidesmosomal lamina lucida and early neutrophil involvement are characteristic features in a case of anti-p200 pemphigoid. / Shimizu, A.; Funakoshi, Takeru; Ishibashi, M.; Yoshida, Tadashi; Koga, H.; Hashimoto, T.; Amagai, Masayuki; Ishiko, A.

In: British Journal of Dermatology, Vol. 168, No. 3, 03.2013, p. 647-655.

Research output: Contribution to journalArticle

@article{ef074b5b71804ccd856d8a4a5f19e058,
title = "Immunoglobulin G deposition to nonhemidesmosomal lamina lucida and early neutrophil involvement are characteristic features in a case of anti-p200 pemphigoid",
abstract = "The ultrastructural characteristics and immunolocalization of in vivo 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 antip200 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 in vivo, 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.",
author = "A. Shimizu and Takeru Funakoshi and M. Ishibashi and Tadashi Yoshida and H. Koga and T. Hashimoto and Masayuki Amagai and A. Ishiko",
year = "2013",
month = "3",
doi = "10.1111/bjd.12033",
language = "English",
volume = "168",
pages = "647--655",
journal = "British Journal of Dermatology",
issn = "0007-0963",
publisher = "Wiley-Blackwell",
number = "3",

}

TY - JOUR

T1 - Immunoglobulin G deposition to nonhemidesmosomal lamina lucida and early neutrophil involvement are characteristic features in a case of anti-p200 pemphigoid

AU - Shimizu, A.

AU - Funakoshi, Takeru

AU - Ishibashi, M.

AU - Yoshida, Tadashi

AU - Koga, H.

AU - Hashimoto, T.

AU - Amagai, Masayuki

AU - Ishiko, A.

PY - 2013/3

Y1 - 2013/3

N2 - The ultrastructural characteristics and immunolocalization of in vivo 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 antip200 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 in vivo, 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.

AB - The ultrastructural characteristics and immunolocalization of in vivo 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 antip200 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 in vivo, 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.

UR - http://www.scopus.com/inward/record.url?scp=84882253027&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84882253027&partnerID=8YFLogxK

U2 - 10.1111/bjd.12033

DO - 10.1111/bjd.12033

M3 - Article

VL - 168

SP - 647

EP - 655

JO - British Journal of Dermatology

JF - British Journal of Dermatology

SN - 0007-0963

IS - 3

ER -