Molecular and Cellular Mechanisms in Skin Disorders

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: 30 October 2025 | Viewed by 910

Special Issue Editor

Special Issue Information

Dear Colleagues,

The skin is one of the largest immune organs involving innate and acquired immune systems. Thus, it can respond to exogenous stimuli by producing large amounts of proinflammatory cytokines, resulting in systemic inflammation.

In psoriasis, one of the intractable inflammatory cytokine-mediated skin disorders, the average life span is six years shorter than the population without a history of psoriasis due to cerebrovascular and cardiovascular complications. Patients with severe eczema also have an increased risk of cardiovascular disorders. Several studies have shown that severe inflammatory skin disorders are strongly associated with systemic complications such as arteriosclerosis, cardiomyopathy, abnormal lipid metabolism, nonalcoholic fatty liver disease, renal sclerosis, and systemic amyloidosis. This has led to the concept of the "inflammatory skin march", highlighting the investigation of molecular and cellular mechanisms of skin disorders and the intimate relationship between skin inflammation and systemic complications.

In this context, we welcome clinical evidence and research findings focusing on molecular and cellular mechanisms of skin diseases, as well as systemic inflammatory changes and systemic organ diseases complicated by inflammatory skin disorders.

Prof. Dr. Keiichi Yamanaka
Guest Editor

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Keywords

  • inflammatory skin disease
  • psoriasis
  • atopic dermatitis
  • cytokine
  • comorbidity
  • complication
  • systemic inflammation
  • internal organ

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Published Papers (1 paper)

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Research

18 pages, 15349 KiB  
Article
Enhanced Innate Immunity Mediated by IL-36α in Atopic Dermatitis and Differences in Cytokine Profiles of Lymphocytes in the Skin and Draining Lymph Nodes
by Ayaka Ichikawa, Mai Nishimura, Masako Ichishi, Yasutomo Imai, Yoshiaki Matsushima, Yoichiro Iwakura, Masatoshi Watanabe, Kiyofumi Yamanishi and Keiichi Yamanaka
Biomolecules 2025, 15(6), 817; https://doi.org/10.3390/biom15060817 - 4 Jun 2025
Viewed by 643
Abstract
(1) Background: The IL-36 cytokines have been identified as key contributors to pustular psoriasis, and their inhibitor is already in clinical use. However, few studies have explored them in atopic dermatitis. (2) Methods: The role of IL-36α was investigated in various atopic dermatitis [...] Read more.
(1) Background: The IL-36 cytokines have been identified as key contributors to pustular psoriasis, and their inhibitor is already in clinical use. However, few studies have explored them in atopic dermatitis. (2) Methods: The role of IL-36α was investigated in various atopic dermatitis models using wild-type, keratin 14-specific IL-33 transgenic, IL-18 transgenic, caspase-1 transgenic, and caspase-1 transgenic mice with IL-17AF deletion, reflecting diverse aspects of human skin inflammation. IL-36α was administered subcutaneously in five doses on alternate days across the five strains to examine cellular infiltration patterns and cytokine expression levels. (3) Results: The skin phenotype was exacerbated, accompanied by worsening edema and skin thickness in all mouse groups upon IL-36α administration. An increase in infiltrating cells was observed among innate immune cells, while lymphocyte counts, including T cells and innate lymphoid cells, did not rise. Additionally, anti-inflammatory cytokines were induced simultaneously with inflammatory cytokines and downstream cytokines of IL-36α as well. Infiltrating lymphocytes in the skin displayed a distinct Type 2 cytokine-dominant profile for innate lymphoid cells and a Type 3 cytokine-dominant profile for T helper cells and γδ T cells, contrasting with the Type 1-dominant cell profile in draining lymph nodes. Type 1, Type 2, and Type 3 cytokine dominance patterns were not affected by the administration of IL-36α. (4) Conclusions: IL-36α triggers inflammatory responses in atopic dermatitis by activating innate immunity. The infiltrating lymphocytes in the skin have different cytokine production profiles between innate lymphoid cells and T cells, as well as different patterns of cytokine production in their draining lymph nodes. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanisms in Skin Disorders)
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