Distinct behavior of human Langerhans cells and inflammatory dendritic epidermal cells at tight junctions in patients with atopic dermatitis
The stratum corneum and tight junctions (TJs) form physical barriers in the epidermis. Dendrites of activated Langerhans cells (LCs) extend beyond the TJs to capture external antigens in mice. LCs and inflammatory dendritic epidermal cells (IDECs) are observed in the skin of patients with atopic der...
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| Published in | Journal of allergy and clinical immunology Vol. 134; no. 4; pp. 856 - 864 |
|---|---|
| Main Authors | , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
New York, NY
Elsevier Inc
01.10.2014
Elsevier Elsevier Limited |
| Subjects | |
| Online Access | Get full text |
| ISSN | 0091-6749 1097-6825 1097-6825 |
| DOI | 10.1016/j.jaci.2014.08.001 |
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| Abstract | The stratum corneum and tight junctions (TJs) form physical barriers in the epidermis. Dendrites of activated Langerhans cells (LCs) extend beyond the TJs to capture external antigens in mice. LCs and inflammatory dendritic epidermal cells (IDECs) are observed in the skin of patients with atopic dermatitis (AD).
We sought to investigate the characteristics of LCs and IDECs and the distribution of their antigen capture receptors in relation to TJs in normal and AD skin.
We characterized the interactions of LCs and IDECs with TJs and the expression patterns of langerin and FcεRI by using whole-mount epidermal sheets from healthy subjects and patients with AD, ichthyosis vulgaris, and psoriasis vulgaris.
As in mouse skin, activated LCs penetrate TJs in human skin. The number of LCs with TJ penetration increased approximately 5-fold in erythematous lesional skin of patients with AD but not in nonlesional skin of patients with AD or lesions of patients with ichthyosis vulgaris or psoriasis. In contrast, IDECs localized in the lower part of the epidermis, and their dendrites extended horizontally without penetration through TJs. Although langerin accumulated on the tips of dendrites of activated LCs, FcεRI was expressed diffusely on the cell surfaces on LCs and IDECs in lesional skin from patients with AD.
These findings highlight interesting differences between LCs and IDECs in epidermis of patients with AD, where LCs, but not IDECs, extend dendrites through the TJs, likely to capture antigens from outside the TJ barrier with a polarized distribution of langerin but not FcεRI. These behavioral differences between skin dendritic cells might reflect an important pathophysiology of AD. |
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| AbstractList | The stratum corneum and tight junctions (TJs) form physical barriers in the epidermis. Dendrites of activated Langerhans cells (LCs) extend beyond the TJs to capture external antigens in mice. LCs and inflammatory dendritic epidermal cells (IDECs) are observed in the skin of patients with atopic dermatitis (AD).
We sought to investigate the characteristics of LCs and IDECs and the distribution of their antigen capture receptors in relation to TJs in normal and AD skin.
We characterized the interactions of LCs and IDECs with TJs and the expression patterns of langerin and FcεRI by using whole-mount epidermal sheets from healthy subjects and patients with AD, ichthyosis vulgaris, and psoriasis vulgaris.
As in mouse skin, activated LCs penetrate TJs in human skin. The number of LCs with TJ penetration increased approximately 5-fold in erythematous lesional skin of patients with AD but not in nonlesional skin of patients with AD or lesions of patients with ichthyosis vulgaris or psoriasis. In contrast, IDECs localized in the lower part of the epidermis, and their dendrites extended horizontally without penetration through TJs. Although langerin accumulated on the tips of dendrites of activated LCs, FcεRI was expressed diffusely on the cell surfaces on LCs and IDECs in lesional skin from patients with AD.
These findings highlight interesting differences between LCs and IDECs in epidermis of patients with AD, where LCs, but not IDECs, extend dendrites through the TJs, likely to capture antigens from outside the TJ barrier with a polarized distribution of langerin but not FcεRI. These behavioral differences between skin dendritic cells might reflect an important pathophysiology of AD. Background The stratum corneum and tight junctions (TJs) form physical barriers in the epidermis. Dendrites of activated Langerhans cells (LCs) extend beyond the TJs to capture external antigens in mice. LCs and inflammatory dendritic epidermal cells (IDECs) are observed in the skin of patients with atopic dermatitis (AD). Objective We sought to investigate the characteristics of LCs and IDECs and the distribution of their antigen capture receptors in relation to TJs in normal and AD skin. Methods We characterized the interactions of LCs and IDECs with TJs and the expression patterns of langerin and FcεRI by using whole-mount epidermal sheets from healthy subjects and patients with AD, ichthyosis vulgaris, and psoriasis vulgaris. Results As in mouse skin, activated LCs penetrate TJs in human skin. The number of LCs with TJ penetration increased approximately 5-fold in erythematous lesional skin of patients with AD but not in nonlesional skin of patients with AD or lesions of patients with ichthyosis vulgaris or psoriasis. In contrast, IDECs localized in the lower part of the epidermis, and their dendrites extended horizontally without penetration through TJs. Although langerin accumulated on the tips of dendrites of activated LCs, FcεRI was expressed diffusely on the cell surfaces on LCs and IDECs in lesional skin from patients with AD. Conclusions These findings highlight interesting differences between LCs and IDECs in epidermis of patients with AD, where LCs, but not IDECs, extend dendrites through the TJs, likely to capture antigens from outside the TJ barrier with a polarized distribution of langerin but not FcεRI. These behavioral differences between skin dendritic cells might reflect an important pathophysiology of AD. The stratum corneum and tight junctions (TJs) form physical barriers in the epidermis. Dendrites of activated Langerhans cells (LCs) extend beyond the TJs to capture external antigens in mice. LCs and inflammatory dendritic epidermal cells (IDECs) are observed in the skin of patients with atopic dermatitis (AD).BACKGROUNDThe stratum corneum and tight junctions (TJs) form physical barriers in the epidermis. Dendrites of activated Langerhans cells (LCs) extend beyond the TJs to capture external antigens in mice. LCs and inflammatory dendritic epidermal cells (IDECs) are observed in the skin of patients with atopic dermatitis (AD).We sought to investigate the characteristics of LCs and IDECs and the distribution of their antigen capture receptors in relation to TJs in normal and AD skin.OBJECTIVEWe sought to investigate the characteristics of LCs and IDECs and the distribution of their antigen capture receptors in relation to TJs in normal and AD skin.We characterized the interactions of LCs and IDECs with TJs and the expression patterns of langerin and FcεRI by using whole-mount epidermal sheets from healthy subjects and patients with AD, ichthyosis vulgaris, and psoriasis vulgaris.METHODSWe characterized the interactions of LCs and IDECs with TJs and the expression patterns of langerin and FcεRI by using whole-mount epidermal sheets from healthy subjects and patients with AD, ichthyosis vulgaris, and psoriasis vulgaris.As in mouse skin, activated LCs penetrate TJs in human skin. The number of LCs with TJ penetration increased approximately 5-fold in erythematous lesional skin of patients with AD but not in nonlesional skin of patients with AD or lesions of patients with ichthyosis vulgaris or psoriasis. In contrast, IDECs localized in the lower part of the epidermis, and their dendrites extended horizontally without penetration through TJs. Although langerin accumulated on the tips of dendrites of activated LCs, FcεRI was expressed diffusely on the cell surfaces on LCs and IDECs in lesional skin from patients with AD.RESULTSAs in mouse skin, activated LCs penetrate TJs in human skin. The number of LCs with TJ penetration increased approximately 5-fold in erythematous lesional skin of patients with AD but not in nonlesional skin of patients with AD or lesions of patients with ichthyosis vulgaris or psoriasis. In contrast, IDECs localized in the lower part of the epidermis, and their dendrites extended horizontally without penetration through TJs. Although langerin accumulated on the tips of dendrites of activated LCs, FcεRI was expressed diffusely on the cell surfaces on LCs and IDECs in lesional skin from patients with AD.These findings highlight interesting differences between LCs and IDECs in epidermis of patients with AD, where LCs, but not IDECs, extend dendrites through the TJs, likely to capture antigens from outside the TJ barrier with a polarized distribution of langerin but not FcεRI. These behavioral differences between skin dendritic cells might reflect an important pathophysiology of AD.CONCLUSIONSThese findings highlight interesting differences between LCs and IDECs in epidermis of patients with AD, where LCs, but not IDECs, extend dendrites through the TJs, likely to capture antigens from outside the TJ barrier with a polarized distribution of langerin but not FcεRI. These behavioral differences between skin dendritic cells might reflect an important pathophysiology of AD. Background The stratum corneum and tight junctions (TJs) form physical barriers in the epidermis. Dendrites of activated Langerhans cells (LCs) extend beyond the TJs to capture external antigens in mice. LCs and inflammatory dendritic epidermal cells (IDECs) are observed in the skin of patients with atopic dermatitis (AD). Objective We sought to investigate the characteristics of LCs and IDECs and the distribution of their antigen capture receptors in relation to TJs in normal and AD skin. Methods We characterized the interactions of LCs and IDECs with TJs and the expression patterns of langerin and Fc[straight epsilon]RI by using whole-mount epidermal sheets from healthy subjects and patients with AD, ichthyosis vulgaris, and psoriasis vulgaris. Results As in mouse skin, activated LCs penetrate TJs in human skin. The number of LCs with TJ penetration increased approximately 5-fold in erythematous lesional skin of patients with AD but not in nonlesional skin of patients with AD or lesions of patients with ichthyosis vulgaris or psoriasis. In contrast, IDECs localized in the lower part of the epidermis, and their dendrites extended horizontally without penetration through TJs. Although langerin accumulated on the tips of dendrites of activated LCs, Fc[straight epsilon]RI was expressed diffusely on the cell surfaces on LCs and IDECs in lesional skin from patients with AD. Conclusions These findings highlight interesting differences between LCs and IDECs in epidermis of patients with AD, where LCs, but not IDECs, extend dendrites through the TJs, likely to capture antigens from outside the TJ barrier with a polarized distribution of langerin but not Fc[straight epsilon]RI. These behavioral differences between skin dendritic cells might reflect an important pathophysiology of AD. Background The stratum corneum and tight junctions (TJs) form physical barriers in the epidermis. Dendrites of activated Langerhans cells (LCs) extend beyond the TJs to capture external antigens in mice. LCs and inflammatory dendritic epidermal cells (IDECs) are observed in the skin of patients with atopic dermatitis (AD). Objective We sought to investigate the characteristics of LCs and IDECs and the distribution of their antigen capture receptors in relation to TJs in normal and AD skin. Methods We characterized the interactions of LCs and IDECs with TJs and the expression patterns of langerin and Fc epsilon RI by using whole-mount epidermal sheets from healthy subjects and patients with AD, ichthyosis vulgaris, and psoriasis vulgaris. Results As in mouse skin, activated LCs penetrate TJs in human skin. The number of LCs with TJ penetration increased approximately 5-fold in erythematous lesional skin of patients with AD but not in nonlesional skin of patients with AD or lesions of patients with ichthyosis vulgaris or psoriasis. In contrast, IDECs localized in the lower part of the epidermis, and their dendrites extended horizontally without penetration through TJs. Although langerin accumulated on the tips of dendrites of activated LCs, Fc epsilon RI was expressed diffusely on the cell surfaces on LCs and IDECs in lesional skin from patients with AD. Conclusions These findings highlight interesting differences between LCs and IDECs in epidermis of patients with AD, where LCs, but not IDECs, extend dendrites through the TJs, likely to capture antigens from outside the TJ barrier with a polarized distribution of langerin but not Fc epsilon RI. These behavioral differences between skin dendritic cells might reflect an important pathophysiology of AD. |
| Author | Nagao, Keisuke Ishii, Ken Kubo, Akiharu Ebihara, Tamotsu Kawasaki, Hiroshi Nomura, Toshifumi Fujita, Harumi Kouyama, Keisuke Yoshida, Kazue Shimizu, Hiroshi Yokouchi, Mariko Amagai, Masayuki |
| Author_xml | – sequence: 1 givenname: Kazue surname: Yoshida fullname: Yoshida, Kazue organization: Department of Dermatology, Keio University School of Medicine, Tokyo, Japan – sequence: 2 givenname: Akiharu surname: Kubo fullname: Kubo, Akiharu email: akiharu@a5.keio.jp organization: Department of Dermatology, Keio University School of Medicine, Tokyo, Japan – sequence: 3 givenname: Harumi surname: Fujita fullname: Fujita, Harumi organization: Department of Dermatology, Keio University School of Medicine, Tokyo, Japan – sequence: 4 givenname: Mariko surname: Yokouchi fullname: Yokouchi, Mariko organization: Department of Dermatology, Keio University School of Medicine, Tokyo, Japan – sequence: 5 givenname: Ken surname: Ishii fullname: Ishii, Ken organization: Department of Dermatology, Keio University School of Medicine, Tokyo, Japan – sequence: 6 givenname: Hiroshi surname: Kawasaki fullname: Kawasaki, Hiroshi organization: Department of Dermatology, Keio University School of Medicine, Tokyo, Japan – sequence: 7 givenname: Toshifumi surname: Nomura fullname: Nomura, Toshifumi organization: Department of Dermatology, Hokkaido University Graduate School of Medicine, Sapporo, Japan – sequence: 8 givenname: Hiroshi surname: Shimizu fullname: Shimizu, Hiroshi organization: Department of Dermatology, Hokkaido University Graduate School of Medicine, Sapporo, Japan – sequence: 9 givenname: Keisuke surname: Kouyama fullname: Kouyama, Keisuke organization: Center for Clinical Research, Keio University School of Medicine, Tokyo, Japan – sequence: 10 givenname: Tamotsu surname: Ebihara fullname: Ebihara, Tamotsu organization: Department of Dermatology, Keio University School of Medicine, Tokyo, Japan – sequence: 11 givenname: Keisuke surname: Nagao fullname: Nagao, Keisuke organization: Department of Dermatology, Keio University School of Medicine, Tokyo, Japan – sequence: 12 givenname: Masayuki surname: Amagai fullname: Amagai, Masayuki organization: Department of Dermatology, Keio University School of Medicine, Tokyo, Japan |
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| Copyright | 2014 American Academy of Allergy, Asthma & Immunology American Academy of Allergy, Asthma & Immunology 2015 INIST-CNRS Copyright © 2014 American Academy of Allergy, Asthma & Immunology. Published by Elsevier Inc. All rights reserved. Copyright Elsevier Limited Oct 2014 |
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| Keywords | AD atopic dermatitis langerin IV SC stratum corneum Biotin-SH 3D ZO-1 Langerhans cell TJ LC FcεRI IDEC inflammatory dendritic epidermal cell tight junction DC Dendritic cell Ichthyosis vulgaris EZ-Link Sulfo-NHS-LC-Biotin Three-dimensional Zonula occludens 1 Human Allergy Immunopathology Skin disease Stratum corneum FcεRI receptor Immunoglobulin receptor Cell junction Inflammation Atopy Immunology Antigen presenting cell Atopic dermatitis Tight junction Inflammatory cell Behavior |
| Language | English |
| License | https://www.elsevier.com/tdm/userlicense/1.0 CC BY 4.0 Copyright © 2014 American Academy of Allergy, Asthma & Immunology. Published by Elsevier Inc. All rights reserved. |
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| Snippet | The stratum corneum and tight junctions (TJs) form physical barriers in the epidermis. Dendrites of activated Langerhans cells (LCs) extend beyond the TJs to... Background The stratum corneum and tight junctions (TJs) form physical barriers in the epidermis. Dendrites of activated Langerhans cells (LCs) extend beyond... |
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| SubjectTerms | Allergic diseases Allergies Allergy and Immunology Animals Antigen Presentation Antigens Antigens, CD - genetics Antigens, CD - metabolism Asthma atopic dermatitis Behavior Biological and medical sciences Biopsy Cell Movement Cells, Cultured Dendritic Cells - immunology Dermatitis, Atopic - complications Dermatitis, Atopic - immunology Epidermis - pathology FcεRI Fundamental and applied biological sciences. Psychology Fundamental immunology Humans Ichthyosis Vulgaris - complications Ichthyosis Vulgaris - immunology Immunopathology inflammatory dendritic epidermal cell Langerhans cell Langerhans Cells - immunology langerin Lectins, C-Type - genetics Lectins, C-Type - metabolism Mannose-Binding Lectins - genetics Mannose-Binding Lectins - metabolism Medical sciences Methods Mice Microscopy, Electron, Scanning Mutation Organ Culture Techniques Psoriasis - complications Psoriasis - immunology Receptors, IgE - genetics Receptors, IgE - metabolism Sarcoidosis. Granulomatous diseases of unproved etiology. Connective tissue diseases. Elastic tissue diseases. Vasculitis Skin Skin allergic diseases. Stinging insect allergies stratum corneum tight junction Tight Junctions - metabolism Tight Junctions - pathology Tight Junctions - ultrastructure Transcriptome Wound healing |
| Title | Distinct behavior of human Langerhans cells and inflammatory dendritic epidermal cells at tight junctions in patients with atopic dermatitis |
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