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Molecular Studies of Dermatitis: From Mechanism to Therapy
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Molecular Studies of Dermatitis: From Mechanism to Therapy

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Immunology".

Deadline for manuscript submissions: 30 May 2024 | Viewed by 10071

Special Issue Editor

Dr. Tokio Nakada

E-Mail Website
Guest Editor
Showa University Fujigaoka Hospital, Yokohama 227-8501, Japan
Interests: contact dermatitis; the innate immune system; T cells; inflammation; cutaneous immunology

Special Issue Information

Dear Colleagues,

Dermatitis represents a group of diseases that cause skin inflammation and histopathological spongiosis. Recently, some studies have demonstrated the presence of factors that had not been associated with the pathophysiology of dermatitis, e.g., damage-associated molecular patterns, various cytokines, etc. For example, the innate immune system plays an important role in irritant and allergic contact dermatitis. Atopic dermatitis is not just an allergic reaction, but a multifocal disease with multiple etiologies consisting of abnormalities of the horny cell layer, inflammation mainly caused by a type 2 immune reaction, and pruritus. It is very interesting to examine new findings in other dermatitis diseases, for example, the roles of epidermal cells, lymphocytes, eosinophils, basophils, mast cells, and macrophages. For this Special Issue, we welcome original research and review articles that focus on these topics.

Dr. Tokio Nakada
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • dermatitis
  • the innate immune system
  • cytokine

Published Papers (6 papers)

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Editorial

Jump to: Research, Review

3 pages, 144 KiB  
Editorial
Special Issue “Molecular Studies of Dermatitis: From Mechanism to Therapy”
by Tokio Nakada
Int. J. Mol. Sci. 2024, 25(5), 2696; https://doi.org/10.3390/ijms25052696 - 26 Feb 2024
Viewed by 355
Abstract
Dermatitis (eczema) represents a group of inflammatory cutaneous diseases [...] Full article
(This article belongs to the Special Issue Molecular Studies of Dermatitis: From Mechanism to Therapy)

Research

Jump to: Editorial, Review

9 pages, 1751 KiB  
Communication
IL-31RA and TRPV1 Expression in Atopic Dermatitis Induced with Trinitrochlorobenzene in Nc/Nga Mice
by Seokwoo Lee, Na Yeon Lim, Min Soo Kang, Yunho Jeong, Jin-Ok Ahn, Jung Hoon Choi and Jin-Young Chung
Int. J. Mol. Sci. 2023, 24(17), 13521; https://doi.org/10.3390/ijms241713521 - 31 Aug 2023
Cited by 2 | Viewed by 1000
Abstract
Atopic dermatitis (AD) is a common chronic inflammatory skin disease. Interleukin 31 (IL-31), a novel cytokine in AD, causes pruritus, typically characteristic of AD patients. The transient receptor potential vanilloid type 1 (TRPV1) is a cation channel activated by diverse noxious stimuli that [...] Read more.
Atopic dermatitis (AD) is a common chronic inflammatory skin disease. Interleukin 31 (IL-31), a novel cytokine in AD, causes pruritus, typically characteristic of AD patients. The transient receptor potential vanilloid type 1 (TRPV1) is a cation channel activated by diverse noxious stimuli that has been studied in a variety of pruritic skin diseases. In this study, the AD animal model was generated by administering the hapten, trinitrochlorobenzene (TNCB), to Nc/Nga mice, and the degree of expression of the IL-31 receptor alpha (IL-31RA) and TRPV1 in the skin of these atopic models was evaluated. The Nc/Nga mice were divided into 3 groups: control, TNCB 2-weeks treated, and TNCB 8-weeks treated. After inducing AD, the skin lesions in each group were scored and compared, and the histology of the skin lesions and the IL-31RA and TRPV1 expression for each group were evaluated by analyzing immunohistochemistry. The results show a significant difference in the skin lesion scores between the groups. The immunohistochemistry evaluation highlighted the remarkable expression of IL-31RA and TRPV1 in the nerve fibers of the TNCB 8-weeks-treated group. We thus confirmed that the long-term application of TNCB induced chronic atopic-like dermatitis and that IL-31RA and TRPV1 were overexpressed in the peripheral nerve fibers in this AD model. Full article
(This article belongs to the Special Issue Molecular Studies of Dermatitis: From Mechanism to Therapy)
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Review

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16 pages, 1600 KiB  
Review
The Involvement of Cysteine-X-Cysteine Motif Chemokine Receptors in Skin Homeostasis and the Pathogenesis of Allergic Contact Dermatitis and Psoriasis
by Wenjie Liu
Int. J. Mol. Sci. 2024, 25(2), 1005; https://doi.org/10.3390/ijms25021005 - 13 Jan 2024
Cited by 1 | Viewed by 913
Abstract
Members of the C-X-C motif chemokine receptor (CXCR) superfamily play central roles in initiating the innate immune response in mammalian cells by orchestrating selective cell migration and immune cell activation. With its multilayered structure, the skin, which is the largest organ in the [...] Read more.
Members of the C-X-C motif chemokine receptor (CXCR) superfamily play central roles in initiating the innate immune response in mammalian cells by orchestrating selective cell migration and immune cell activation. With its multilayered structure, the skin, which is the largest organ in the body, performs a crucial defense function, protecting the human body from harmful environmental threats and pathogens. CXCRs contribute to primary immunological defense; these receptors are differentially expressed by different types of skin cells and act as key players in initiating downstream innate immune responses. While the initiation of inflammatory responses by CXCRs is essential for pathogen elimination and tissue healing, overactivation of these receptors can enhance T-cell-mediated autoimmune responses, resulting in excessive inflammation and the development of several skin disorders, including psoriasis, atopic dermatitis, allergic contact dermatitis, vitiligo, autoimmune diseases, and skin cancers. In summary, CXCRs serve as critical links that connect innate immunity and adaptive immunity. In this article, we present the current knowledge about the functions of CXCRs in the homeostasis function of the skin and their contributions to the pathogenesis of allergic contact dermatitis and psoriasis. Furthermore, we will examine the research progress and efficacy of therapeutic approaches that target CXCRs. Full article
(This article belongs to the Special Issue Molecular Studies of Dermatitis: From Mechanism to Therapy)
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11 pages, 1341 KiB  
Review
New Perspectives in the Management of Chronic Hand Eczema: Lessons from Pathogenesis
by Vittorio Tancredi, Dario Buononato, Stefano Caccavale, Eugenia Veronica Di Brizzi, Roberta Di Caprio, Giuseppe Argenziano and Anna Balato
Int. J. Mol. Sci. 2024, 25(1), 362; https://doi.org/10.3390/ijms25010362 - 27 Dec 2023
Viewed by 1365
Abstract
Chronic hand eczema (CHE) is a common inflammatory skin condition that significantly impacts the quality of life. From work-related disabilities to social embarrassment, pain, and financial costs, the burden on society is substantial. Managing this condition presents challenges such as long-term treatment, poor [...] Read more.
Chronic hand eczema (CHE) is a common inflammatory skin condition that significantly impacts the quality of life. From work-related disabilities to social embarrassment, pain, and financial costs, the burden on society is substantial. Managing this condition presents challenges such as long-term treatment, poor patient compliance, therapy side effects, and economic feasibility. As a result, significant efforts have been made in this field in recent years. Specifically, the broader understanding of CHE pathogenesis has led to the development of new drugs, both topical and systemic. The aim of this narrative review is to summarize the current available data on hand eczema pathophysiology and explore the resulting developments in drugs for its treatment. A comprehensive search on PubMed and the other main scientific databases was conducted using keywords related to CHE and its pathogenesis. The most relevant pathways targeted by therapies include the JAK-STAT cascade, IL-4, and IL-13 axis, phosphodiesterase 4 enzyme, and chemo-attractant cytokines. In the near future, physicians will have a plethora of therapeutic alternatives. Consequently, they should be well-trained not only in how to use these alternatives but also how to combine these treatments to address the ongoing challenges related to efficacy, tolerability, and safety. Full article
(This article belongs to the Special Issue Molecular Studies of Dermatitis: From Mechanism to Therapy)
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27 pages, 3570 KiB  
Review
Role of Innate Immunity in Allergic Contact Dermatitis: An Update
by Hiroki L. Yamaguchi, Yuji Yamaguchi and Elena Peeva
Int. J. Mol. Sci. 2023, 24(16), 12975; https://doi.org/10.3390/ijms241612975 - 19 Aug 2023
Cited by 5 | Viewed by 3217
Abstract
Our understanding of allergic contact dermatitis mechanisms has progressed over the past decade. Innate immune cells that are involved in the pathogenesis of allergic contact dermatitis include Langerhans cells, dermal dendritic cells, macrophages, mast cells, innate lymphoid cells (ILCs), neutrophils, eosinophils, and basophils. [...] Read more.
Our understanding of allergic contact dermatitis mechanisms has progressed over the past decade. Innate immune cells that are involved in the pathogenesis of allergic contact dermatitis include Langerhans cells, dermal dendritic cells, macrophages, mast cells, innate lymphoid cells (ILCs), neutrophils, eosinophils, and basophils. ILCs can be subcategorized as group 1 (natural killer cells; ILC1) in association with Th1, group 2 (ILC2) in association with Th2, and group 3 (lymphoid tissue-inducer cells; ILC3) in association with Th17. Pattern recognition receptors (PRRs) including toll-like receptors (TLRs) and nucleotide-binding oligomerization domain (NOD)-like receptors (NLRs) in innate immune cells recognize damage-associated molecular patterns (DAMPs) and cascade the signal to produce several cytokines and chemokines including tumor necrosis factor (TNF)-α, interferon (IFN)-α, IFN-γ, interleukin (IL)-1β, IL-4, IL-6, IL-12, IL-13, IL-17, IL-18, and IL-23. Here we discuss the recent findings showing the roles of the innate immune system in allergic contact dermatitis during the sensitization and elicitation phases. Full article
(This article belongs to the Special Issue Molecular Studies of Dermatitis: From Mechanism to Therapy)
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13 pages, 718 KiB  
Review
Contact Dermatitis to Diabetes Medical Devices
by Mikołaj Cichoń, Magdalena Trzeciak, Małgorzata Sokołowska-Wojdyło and Roman J. Nowicki
Int. J. Mol. Sci. 2023, 24(13), 10697; https://doi.org/10.3390/ijms241310697 - 27 Jun 2023
Cited by 4 | Viewed by 2404
Abstract
Skin adverse reactions to diabetes medical devices have been reported frequently over recent years. Adhesives attaching glucose sensors and continuous insulin infusion sets to the skin are proven to cause both allergic contact dermatitis and irritant contact dermatitis in patients with diabetes mellitus. [...] Read more.
Skin adverse reactions to diabetes medical devices have been reported frequently over recent years. Adhesives attaching glucose sensors and continuous insulin infusion sets to the skin are proven to cause both allergic contact dermatitis and irritant contact dermatitis in patients with diabetes mellitus. Several allergens contained in adhesives and/or parts of medical devices are documented to cause allergic contact dermatitis, with acrylate chemicals being the most common culprit-especially isobornyl acrylate (IBOA), but also 2,2′-methylenebis(6-tert-butyl-4-methylphenol) monoacrylate or cyanoacrylates. Epoxy resin, colophonium and nickel were also identified as causative allergens. However, repetitive occlusion, maceration of the skin and resulting disruption of the skin barrier seem to have an impact on the development of skin lesions as well. The purpose of this study is to highlight the burden of contact dermatitis triggered by diabetes medical devices and to show possible mechanisms responsible for the development of contact dermatitis in a group of diabetic patients. Full article
(This article belongs to the Special Issue Molecular Studies of Dermatitis: From Mechanism to Therapy)
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