Emerging Role of the IL-36/IL-36R Axis in Multiple Inflammatory Skin Diseases
Copyright © 2023 The Authors. Published by Elsevier Inc. All rights reserved..
IL-36 is a most recent member of the IL-1 cytokine family, primarily expressed at barrier sites of the body such as the skin, lungs, and intestine. It plays a vital role in inflammation and is implicated in the development of various cutaneous; intestinal; and pulmonary disorders, including psoriasis, inflammatory bowel disease, and chronic obstructive pulmonary disease. IL-36 comprises 4 isoforms: the proinflammatory IL-36α, IL-36β, and IL-36γ and the anti-inflammatory IL-36R antagonist. An imbalance between proinflammatory and anti-inflammatory IL-36 isoforms can contribute to the inflammatory fate of cells and tissues. IL-36 cytokines signal through an IL-36R heterodimer mediating their function through canonical signaling cacade, including the NF-B pathway. Prominent for its role in psoriasis, IL-36 has recently been associated with disease mechanisms in atopic dermatitis, hidradenitis suppurativa, neutrophilic dermatoses, autoimmune blistering disease, and Netherton syndrome. The major cutaneous source of IL-36 cytokines is keratinocytes, pointing to its role in the communication between the epidermis, innate (neutrophils, dendritic cells) immune system, and adaptive (T helper [Th]1 cells, Th17) immune system. Thus, cutaneous IL-36 signaling is crucial for the immunopathological outcome of various skin diseases. Consequently, the IL-36/IL-36R axis has recently been recognized as a promising drug target for the treatment of inflammatory disorders beyond psoriasis. This review summarizes the current update on IL-36 cytokines in inflammatory skin diseases.
Medienart: |
E-Artikel |
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Erscheinungsjahr: |
2024 |
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Erschienen: |
2024 |
Enthalten in: |
Zur Gesamtaufnahme - volume:144 |
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Enthalten in: |
The Journal of investigative dermatology - 144(2024), 2 vom: 05. Feb., Seite 206-224 |
Sprache: |
Englisch |
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Beteiligte Personen: |
Ahmad, Fareed [VerfasserIn] |
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Anmerkungen: |
Date Completed 06.02.2024 Date Revised 06.02.2024 published: Print-Electronic Citation Status MEDLINE |
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doi: |
10.1016/j.jid.2023.11.004 |
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funding: |
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Förderinstitution / Projekttitel: |
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PPN (Katalog-ID): |
NLM366803271 |
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520 | |a IL-36 is a most recent member of the IL-1 cytokine family, primarily expressed at barrier sites of the body such as the skin, lungs, and intestine. It plays a vital role in inflammation and is implicated in the development of various cutaneous; intestinal; and pulmonary disorders, including psoriasis, inflammatory bowel disease, and chronic obstructive pulmonary disease. IL-36 comprises 4 isoforms: the proinflammatory IL-36α, IL-36β, and IL-36γ and the anti-inflammatory IL-36R antagonist. An imbalance between proinflammatory and anti-inflammatory IL-36 isoforms can contribute to the inflammatory fate of cells and tissues. IL-36 cytokines signal through an IL-36R heterodimer mediating their function through canonical signaling cacade, including the NF-B pathway. Prominent for its role in psoriasis, IL-36 has recently been associated with disease mechanisms in atopic dermatitis, hidradenitis suppurativa, neutrophilic dermatoses, autoimmune blistering disease, and Netherton syndrome. The major cutaneous source of IL-36 cytokines is keratinocytes, pointing to its role in the communication between the epidermis, innate (neutrophils, dendritic cells) immune system, and adaptive (T helper [Th]1 cells, Th17) immune system. Thus, cutaneous IL-36 signaling is crucial for the immunopathological outcome of various skin diseases. Consequently, the IL-36/IL-36R axis has recently been recognized as a promising drug target for the treatment of inflammatory disorders beyond psoriasis. This review summarizes the current update on IL-36 cytokines in inflammatory skin diseases | ||
650 | 4 | |a Journal Article | |
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650 | 4 | |a Atopic Dermatitis | |
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700 | 1 | |a Jochebeth, Anh |e verfasserin |4 aut | |
700 | 1 | |a Leo, Rari |e verfasserin |4 aut | |
700 | 1 | |a Al-Abdulla, Mohammed Nasser |e verfasserin |4 aut | |
700 | 1 | |a Al-Khawaga, Sara |e verfasserin |4 aut | |
700 | 1 | |a AlHammadi, Ayda |e verfasserin |4 aut | |
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700 | 1 | |a Buddenkotte, Jörg |e verfasserin |4 aut | |
700 | 1 | |a Steinhoff, Martin |e verfasserin |4 aut | |
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