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Pathogenic Activation and Therapeutic Blockage of FcαR-Expressing Polymorphonuclear Leukocytes in IgA Pemphigus

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Pathogenic Activation and Therapeutic Blockage of FcαR-Expressing Polymorphonuclear Leukocytes in IgA Pemphigus. / Emtenani, Shirin; Ghorbanalipoor, Saeedeh; Mayer-Hain, Sarah; Kridin, Khalaf; Komorowski, Lars; Probst, Christian; Hashimoto, Takashi; Pas, Hendri H; Męcińska-Jundziłł, Kaja; Czajkowski, Rafał; Recke, Andreas; Sunderkötter, Cord; Schneider, Stefan W; Hundt, Jennifer E; Zillikens, Detlef; Schmidt, Enno; Ludwig, Ralf J; Hammers, Christoph M.

in: J INVEST DERMATOL, Jahrgang 141, Nr. 12, 12.2021, S. 2820-2828.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Emtenani, S, Ghorbanalipoor, S, Mayer-Hain, S, Kridin, K, Komorowski, L, Probst, C, Hashimoto, T, Pas, HH, Męcińska-Jundziłł, K, Czajkowski, R, Recke, A, Sunderkötter, C, Schneider, SW, Hundt, JE, Zillikens, D, Schmidt, E, Ludwig, RJ & Hammers, CM 2021, 'Pathogenic Activation and Therapeutic Blockage of FcαR-Expressing Polymorphonuclear Leukocytes in IgA Pemphigus', J INVEST DERMATOL, Jg. 141, Nr. 12, S. 2820-2828. https://doi.org/10.1016/j.jid.2021.06.007

APA

Emtenani, S., Ghorbanalipoor, S., Mayer-Hain, S., Kridin, K., Komorowski, L., Probst, C., Hashimoto, T., Pas, H. H., Męcińska-Jundziłł, K., Czajkowski, R., Recke, A., Sunderkötter, C., Schneider, S. W., Hundt, J. E., Zillikens, D., Schmidt, E., Ludwig, R. J., & Hammers, C. M. (2021). Pathogenic Activation and Therapeutic Blockage of FcαR-Expressing Polymorphonuclear Leukocytes in IgA Pemphigus. J INVEST DERMATOL, 141(12), 2820-2828. https://doi.org/10.1016/j.jid.2021.06.007

Vancouver

Emtenani S, Ghorbanalipoor S, Mayer-Hain S, Kridin K, Komorowski L, Probst C et al. Pathogenic Activation and Therapeutic Blockage of FcαR-Expressing Polymorphonuclear Leukocytes in IgA Pemphigus. J INVEST DERMATOL. 2021 Dez;141(12):2820-2828. https://doi.org/10.1016/j.jid.2021.06.007

Bibtex

@article{10c7a9fdd8c64c558543a95b1cd598bc,
title = "Pathogenic Activation and Therapeutic Blockage of FcαR-Expressing Polymorphonuclear Leukocytes in IgA Pemphigus",
abstract = "Pathomechanisms in IgA pemphigus are assumed to rely on Fc-dependent cellular activation by antigen-specific IgA autoantibodies; however, models for the disease and more detailed pathophysiologic data are lacking. In this study, we aimed to establish in vitro models of disease for IgA pemphigus, allowing us to study the effects of the interaction of anti-keratinocyte IgA with cell surface FcαRs. Employing multiple in vitro assays, such as a skin cryosection assay and a human skin organ culture model, in this study, we present mechanistic data for the pathogenesis of IgA pemphigus, mediated by anti-desmoglein 3 IgA autoantibodies. Our results reveal that this disease is dependent on FcαR-mediated activation of leukocytes in the epidermis. Importantly, this cell-dependent pathology can be dose-dependently abrogated by peptide-mediated inhibition of FcαR:IgA-Fc interaction, as confirmed in an additional model for IgA-dependent disease, that is, IgA vasculitis. These data suggest that IgA pemphigus can be modeled in vitro and that IgA pemphigus and IgA vasculitis are FcαR-dependent disease entities that can be specifically targeted in these experimental systems.",
keywords = "Antigens, CD/physiology, Desmoglein 3/immunology, Eye Proteins/pharmacology, Humans, Immunoglobulin A/immunology, Neutrophils/physiology, Pemphigus/etiology, Peptide Fragments/pharmacology, Receptors, Fc/antagonists & inhibitors",
author = "Shirin Emtenani and Saeedeh Ghorbanalipoor and Sarah Mayer-Hain and Khalaf Kridin and Lars Komorowski and Christian Probst and Takashi Hashimoto and Pas, {Hendri H} and Kaja M{\c e}ci{\'n}ska-Jundzi{\l}{\l} and Rafa{\l} Czajkowski and Andreas Recke and Cord Sunderk{\"o}tter and Schneider, {Stefan W} and Hundt, {Jennifer E} and Detlef Zillikens and Enno Schmidt and Ludwig, {Ralf J} and Hammers, {Christoph M}",
note = "Copyright {\textcopyright} 2021 The Authors. Published by Elsevier Inc. All rights reserved.",
year = "2021",
month = dec,
doi = "10.1016/j.jid.2021.06.007",
language = "English",
volume = "141",
pages = "2820--2828",
journal = "J INVEST DERMATOL",
issn = "0022-202X",
publisher = "NATURE PUBLISHING GROUP",
number = "12",

}

RIS

TY - JOUR

T1 - Pathogenic Activation and Therapeutic Blockage of FcαR-Expressing Polymorphonuclear Leukocytes in IgA Pemphigus

AU - Emtenani, Shirin

AU - Ghorbanalipoor, Saeedeh

AU - Mayer-Hain, Sarah

AU - Kridin, Khalaf

AU - Komorowski, Lars

AU - Probst, Christian

AU - Hashimoto, Takashi

AU - Pas, Hendri H

AU - Męcińska-Jundziłł, Kaja

AU - Czajkowski, Rafał

AU - Recke, Andreas

AU - Sunderkötter, Cord

AU - Schneider, Stefan W

AU - Hundt, Jennifer E

AU - Zillikens, Detlef

AU - Schmidt, Enno

AU - Ludwig, Ralf J

AU - Hammers, Christoph M

N1 - Copyright © 2021 The Authors. Published by Elsevier Inc. All rights reserved.

PY - 2021/12

Y1 - 2021/12

N2 - Pathomechanisms in IgA pemphigus are assumed to rely on Fc-dependent cellular activation by antigen-specific IgA autoantibodies; however, models for the disease and more detailed pathophysiologic data are lacking. In this study, we aimed to establish in vitro models of disease for IgA pemphigus, allowing us to study the effects of the interaction of anti-keratinocyte IgA with cell surface FcαRs. Employing multiple in vitro assays, such as a skin cryosection assay and a human skin organ culture model, in this study, we present mechanistic data for the pathogenesis of IgA pemphigus, mediated by anti-desmoglein 3 IgA autoantibodies. Our results reveal that this disease is dependent on FcαR-mediated activation of leukocytes in the epidermis. Importantly, this cell-dependent pathology can be dose-dependently abrogated by peptide-mediated inhibition of FcαR:IgA-Fc interaction, as confirmed in an additional model for IgA-dependent disease, that is, IgA vasculitis. These data suggest that IgA pemphigus can be modeled in vitro and that IgA pemphigus and IgA vasculitis are FcαR-dependent disease entities that can be specifically targeted in these experimental systems.

AB - Pathomechanisms in IgA pemphigus are assumed to rely on Fc-dependent cellular activation by antigen-specific IgA autoantibodies; however, models for the disease and more detailed pathophysiologic data are lacking. In this study, we aimed to establish in vitro models of disease for IgA pemphigus, allowing us to study the effects of the interaction of anti-keratinocyte IgA with cell surface FcαRs. Employing multiple in vitro assays, such as a skin cryosection assay and a human skin organ culture model, in this study, we present mechanistic data for the pathogenesis of IgA pemphigus, mediated by anti-desmoglein 3 IgA autoantibodies. Our results reveal that this disease is dependent on FcαR-mediated activation of leukocytes in the epidermis. Importantly, this cell-dependent pathology can be dose-dependently abrogated by peptide-mediated inhibition of FcαR:IgA-Fc interaction, as confirmed in an additional model for IgA-dependent disease, that is, IgA vasculitis. These data suggest that IgA pemphigus can be modeled in vitro and that IgA pemphigus and IgA vasculitis are FcαR-dependent disease entities that can be specifically targeted in these experimental systems.

KW - Antigens, CD/physiology

KW - Desmoglein 3/immunology

KW - Eye Proteins/pharmacology

KW - Humans

KW - Immunoglobulin A/immunology

KW - Neutrophils/physiology

KW - Pemphigus/etiology

KW - Peptide Fragments/pharmacology

KW - Receptors, Fc/antagonists & inhibitors

U2 - 10.1016/j.jid.2021.06.007

DO - 10.1016/j.jid.2021.06.007

M3 - SCORING: Journal article

C2 - 34246620

VL - 141

SP - 2820

EP - 2828

JO - J INVEST DERMATOL

JF - J INVEST DERMATOL

SN - 0022-202X

IS - 12

ER -