Immunoglobulin M pemphigoid

Katharina Boch; Christoph M. Hammers; Stephanie Goletz; Mayumi Kamaguchi; Ralf J. Ludwig; Stefan W. Schneider; Detlef Zillikens; Eva Hadaschik; Enno Schmidt

doi:10.1016/j.jaad.2021.01.017

Immunoglobulin M pemphigoid

Katharina Boch, Christoph M. Hammers, Stephanie Goletz, Mayumi Kamaguchi, Ralf J. Ludwig, Stefan W. Schneider, Detlef Zillikens, Eva Hadaschik, Enno Schmidt^*

^*Corresponding author for this work

27 Citations (Scopus)

Abstract

Background: Pemphigoid diseases are a heterogeneous group of autoimmune blistering disorders characterized by predominant deposition of immunoglobulin G or immunoglobulin A autoantibodies against structural proteins of the dermoepidermal junction (DEJ). Sole linear immunoglobulin M (IgM) deposits at the DEJ in pemphigoid diseases have been observed; however, IgM-specific target antigens have not been identified. Objective: Characterization of patients with IgM pemphigoid. Methods: Skin biopsy specimens and sera from IgM-positive patients were assessed using histopathology, direct and indirect immunofluorescence microscopy, enzyme-linked immunosorbent assays, immunoblotting, cryosection assay, complement fixation test, and internalization assays. Results: Tissue-bound linear IgM deposits along the DEJ and circulating IgM autoantibodies against type XVII collagen (Col17) were detected. These circulating IgM autoantibodies showed no complement activating or blister inducing capacity, but the ability of Col17 internalization ex vivo. Limitations: Limited number of patients. Conclusion: This study provides further evidence for the role of IgM autoantibodies in pemphigoid disease and highlights Col17 as a target antigen in IgM pemphigoid.

Original language	English
Journal	Journal of the American Academy of Dermatology
Volume	85
Issue number	6
Pages (from-to)	1486-1492
Number of pages	7
ISSN	0190-9622
DOIs	https://doi.org/10.1016/j.jaad.2021.01.017
Publication status	Published - 12.2021

Funding

Funding sources: Supported by structural funding from the Deutsche Forschungsgemeinschaft through CRU 303 Pemphigoid Diseases and Excellence Cluster 2167/1 Precision Medicine in Chronic Inflammation (to Drs Ludwig, Zillikens, and Schmidt).We thank Ingeborg Atefi and Marina Kongsbak-Reim, L?beck, Germany, for excellent technical support, and Manuela Pigors for reviewing the manuscript. We are grateful to Christian Probst and Lars Komorowski, Euroimmun, L?beck, Germany, for providing recombinant Col17 proteins.

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

SDG 3 Good Health and Well-being

Research Areas and Centers

Academic Focus: Center for Infection and Inflammation Research (ZIEL)
Centers: Center for Research on Inflammation of the Skin (CRIS)

DFG Research Classification Scheme

2.21-05 Immunology
2.22-19 Dermatology

Access to Document

10.1016/j.jaad.2021.01.017

Cite this

@article{2561e8e6be074608b4171f8f754daec4,

title = "Immunoglobulin M pemphigoid",

abstract = "Background: Pemphigoid diseases are a heterogeneous group of autoimmune blistering disorders characterized by predominant deposition of immunoglobulin G or immunoglobulin A autoantibodies against structural proteins of the dermoepidermal junction (DEJ). Sole linear immunoglobulin M (IgM) deposits at the DEJ in pemphigoid diseases have been observed; however, IgM-specific target antigens have not been identified. Objective: Characterization of patients with IgM pemphigoid. Methods: Skin biopsy specimens and sera from IgM-positive patients were assessed using histopathology, direct and indirect immunofluorescence microscopy, enzyme-linked immunosorbent assays, immunoblotting, cryosection assay, complement fixation test, and internalization assays. Results: Tissue-bound linear IgM deposits along the DEJ and circulating IgM autoantibodies against type XVII collagen (Col17) were detected. These circulating IgM autoantibodies showed no complement activating or blister inducing capacity, but the ability of Col17 internalization ex vivo. Limitations: Limited number of patients. Conclusion: This study provides further evidence for the role of IgM autoantibodies in pemphigoid disease and highlights Col17 as a target antigen in IgM pemphigoid.",

author = "Katharina Boch and Hammers, \{Christoph M.\} and Stephanie Goletz and Mayumi Kamaguchi and Ludwig, \{Ralf J.\} and Schneider, \{Stefan W.\} and Detlef Zillikens and Eva Hadaschik and Enno Schmidt",

note = "Publisher Copyright: {\textcopyright} 2021 American Academy of Dermatology, Inc. Copyright {\textcopyright} 2021 American Academy of Dermatology, Inc. Published by Elsevier Inc. All rights reserved.",

year = "2021",

month = dec,

doi = "10.1016/j.jaad.2021.01.017",

language = "English",

volume = "85",

pages = "1486--1492",

journal = "Journal of the American Academy of Dermatology",

issn = "0190-9622",

publisher = "Elsevier Inc.",

number = "6",

}

TY - JOUR

T1 - Immunoglobulin M pemphigoid

AU - Boch, Katharina

AU - Hammers, Christoph M.

AU - Goletz, Stephanie

AU - Kamaguchi, Mayumi

AU - Ludwig, Ralf J.

AU - Schneider, Stefan W.

AU - Zillikens, Detlef

AU - Hadaschik, Eva

AU - Schmidt, Enno

PY - 2021/12

Y1 - 2021/12

N2 - Background: Pemphigoid diseases are a heterogeneous group of autoimmune blistering disorders characterized by predominant deposition of immunoglobulin G or immunoglobulin A autoantibodies against structural proteins of the dermoepidermal junction (DEJ). Sole linear immunoglobulin M (IgM) deposits at the DEJ in pemphigoid diseases have been observed; however, IgM-specific target antigens have not been identified. Objective: Characterization of patients with IgM pemphigoid. Methods: Skin biopsy specimens and sera from IgM-positive patients were assessed using histopathology, direct and indirect immunofluorescence microscopy, enzyme-linked immunosorbent assays, immunoblotting, cryosection assay, complement fixation test, and internalization assays. Results: Tissue-bound linear IgM deposits along the DEJ and circulating IgM autoantibodies against type XVII collagen (Col17) were detected. These circulating IgM autoantibodies showed no complement activating or blister inducing capacity, but the ability of Col17 internalization ex vivo. Limitations: Limited number of patients. Conclusion: This study provides further evidence for the role of IgM autoantibodies in pemphigoid disease and highlights Col17 as a target antigen in IgM pemphigoid.

AB - Background: Pemphigoid diseases are a heterogeneous group of autoimmune blistering disorders characterized by predominant deposition of immunoglobulin G or immunoglobulin A autoantibodies against structural proteins of the dermoepidermal junction (DEJ). Sole linear immunoglobulin M (IgM) deposits at the DEJ in pemphigoid diseases have been observed; however, IgM-specific target antigens have not been identified. Objective: Characterization of patients with IgM pemphigoid. Methods: Skin biopsy specimens and sera from IgM-positive patients were assessed using histopathology, direct and indirect immunofluorescence microscopy, enzyme-linked immunosorbent assays, immunoblotting, cryosection assay, complement fixation test, and internalization assays. Results: Tissue-bound linear IgM deposits along the DEJ and circulating IgM autoantibodies against type XVII collagen (Col17) were detected. These circulating IgM autoantibodies showed no complement activating or blister inducing capacity, but the ability of Col17 internalization ex vivo. Limitations: Limited number of patients. Conclusion: This study provides further evidence for the role of IgM autoantibodies in pemphigoid disease and highlights Col17 as a target antigen in IgM pemphigoid.

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JF - Journal of the American Academy of Dermatology

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ER -

Immunoglobulin M pemphigoid

Abstract

Funding

UN SDGs

Research Areas and Centers

DFG Research Classification Scheme

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Fingerprint

EXC 2167: Precision Medicine in Chronic Inflammation (PMI)

Cite this

Immunoglobulin M pemphigoid

Abstract

Funding

UN SDGs

Research Areas and Centers

DFG Research Classification Scheme

Access to Document

Other files and links

Fingerprint

Projects

EXC 2167: Precision Medicine in Chronic Inflammation (PMI)

Cite this