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Molecular and Cellular Mechanisms of Skin Diseases (Second Edition)

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

Deadline for manuscript submissions: 20 July 2025 | Viewed by 445

Special Issue Editor


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Guest Editor
Department of Surgical, Medical, Dental and Morphological Sciences, University of Modena and Reggio Emilia, 41124 Modena, Italy
Interests: skin cancer; squamous cell carcinoma; psoriasis; epidermal homeostasis; keratinocyte stem cells; epidermal differentiation; skin inflammation; mouse models; zebrafish models; skin in vitro 3D models; skin tumor spheroids; next-generation sequencing
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Special Issue Information

Dear Colleagues,

In recent years, enormous progress has been made in providing a thorough characterization of dermatological diseases at both the molecular and cellular levels; this is due to the identification of new molecular mechanisms and increasingly technological experimental approaches used for their study.

In particular, the detailed analysis of cell metabolism, proliferation, and differentiation has allowed us to define more accurately cell populations with specific functions, both in the health and pathological contexts. Moreover, the development of new technologies, including NGS and gene editing methods, allows us to decipher the necessary information for obtaining concrete applications for the therapeutical responses that each skin disease needs.

Considering the above facts, this Special Issue is open to receiving research papers, up-to-date review articles, and commentaries related to novel insights into healthy and pathological skin cell and tissue biology, including metabolomic, transcriptomic, or proteomic aspects, as well as inflammation. The use of novel tools, both in vitro and in vivo, such as three-dimensional approaches, is encouraged.

Dr. Elisabetta Palazzo
Guest Editor

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Keywords

  • hyperproliferative skin diseases
  • psoriasis
  • keratinocyte carcinoma
  • actinic keratosis
  • atopic dermatitis
  • skin inflammation
  • inflammation-associated skin diseases
  • epidermal differentiation
  • epidermal cell metabolism
  • 3D models
  • in vivo models

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Published Papers (1 paper)

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Research

16 pages, 5528 KiB  
Article
IL-17 Ligand and Receptor Family Members Are Differentially Expressed by Keratinocyte Subpopulations and Modulate Their Differentiation and Inflammatory Phenotype
by Elisabetta Palazzo, Roberta Lotti, Marika Quadri, Carlo Pincelli and Alessandra Marconi
Int. J. Mol. Sci. 2025, 26(7), 2989; https://doi.org/10.3390/ijms26072989 - 25 Mar 2025
Viewed by 331
Abstract
Psoriasis is a chronic inflammatory skin disease characterized by dysregulation of the interleukin 17 (IL-17) signaling axis. Given that psoriasis development depends on keratinocyte stem cells and early progenitors’ sensitivity to differentiation, we analyzed IL-17 ligands and the expression and function of in [...] Read more.
Psoriasis is a chronic inflammatory skin disease characterized by dysregulation of the interleukin 17 (IL-17) signaling axis. Given that psoriasis development depends on keratinocyte stem cells and early progenitors’ sensitivity to differentiation, we analyzed IL-17 ligands and the expression and function of in a novel subset of keratinocyte subpopulations: keratinocyte stem cells (KSC) and early and late Transit Amplifying (ETA or LTA, respectively) cells. We found that all subpopulations expressed all IL-17 variants, predominantly in ETA and LTA. Conversely, IL-17 receptor expression resulted in more heterogeneity, with IL-17RA, -C, and -E being the most differentially regulated. Stimulus with IL-17A, IL-17-F, IL-17-A/F, and IL-17C promotes the upregulation of CXCL1, CXCL8, and DEFB4 mRNAs expression in both KSC and ETA. Moreover, IL-17A and IL-17A/F mainly decrease KSC proliferation and promote cell cycle block. Globally, IL-17A and IL-17A/F modulated the expression of proliferation, differentiation, and psoriasis-associated markers. Furthermore, KSC- and ETA-derived 3D reconstructions displayed increased epidermal thickness and upregulated KRT16 expression after treatment with IL-17A or IL-17A/F. Therefore, our data demonstrated that IL-17 family members perform distinctive functions in a specific keratinocyte subpopulation and define IL-17 signaling as a critical modulator of KSC behavior, proving its role in epidermal homeostasis dysregulation of psoriasis. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Skin Diseases (Second Edition))
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