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Exploring UV-Induced Disease: Insights into Mechanisms and Innovative Strategies for Prevention and Therapy

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 1 February 2026 | Viewed by 1015

Special Issue Editors


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Guest Editor
Department of Dermatology, Heersink School of Medicine, University of Alabama, Birmingham, AL, USA
Interests: ultraviolet radiation; skin

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Guest Editor
Department of Pharmaceutical Sciences, College of Pharmacy, Western University of Health Sciences, Pomona, CA 91766, USA
Interests: stress-induced skin damage; inflammation; immunosuppression; carcinogenesis

Special Issue Information

Dear Colleagues,

Ultraviolet (UV) radiation is a major source of environmental hazards that we encounter daily. Although UV has beneficial effects, overexposure is detrimental and is considered a major contributing factor in the development of skin cancers. Moreover, UV can also induce inflammatory and autoimmune diseases in the skin. Significant efforts have been made to understand the mechanisms underlying UV-induced skin diseases and to develop preventive and therapeutic strategies. However, many areas of uncertainty are yet to be resolved.

UV-induced DNA damage in skin is not only a key mechanism behind gene mutation but also an important initial factor in inflammation and immunosuppression. Understanding the mechanisms behind UV-induced DNA damage and repair will greatly aid in the prevention of UV-induced diseases. Advances in new technology and big data analysis have provided critical insights into mechanisms in animal models and patient studies. Innovative strategies for preventing UV-induced immunosuppression and enhancing immune responses to tumors will help improve patient care. We also welcome contributions on prevention and treatment strategies for ultraviolet-related diseases, even if their mechanisms are not exclusively centered on ultraviolet radiation.

Dr. Hui Xu
Prof. Dr. Ying Huang
Guest Editors

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Keywords

  • ultraviolet radiation
  • skin
  • DNA damage
  • DNA repair
  • immunosuppression
  • inflammatory disease
  • autoimmune disease
  • melanoma
  • non-melanoma skin cancers
  • genetic susceptibility
  • chemopre-vention
  • tumor immunotherapy
  • skin organoids for UV study
  • new animal models

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Published Papers (1 paper)

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Research

11 pages, 2186 KB  
Article
MyD88 Plays an Important Role in UVB-Induced Suppression of Dendritic Cell Activity, T Cell Function, and Cutaneous Immune Response
by Mohammad Asif Sherwani, Carlos Alberto Mier Aguilar, Charlotte McRae, Gelare Ghajar-Rahimi, Aisha Anwaar, Ahmed Omar Jasser, Ariq Chandra, Hui Xu and Nabiha Yusuf
Int. J. Mol. Sci. 2025, 26(19), 9361; https://doi.org/10.3390/ijms26199361 - 25 Sep 2025
Viewed by 803
Abstract
Ultraviolet B (UVB) radiation triggers DNA damage and immune suppression, establishing conditions favorable for skin carcinogenesis. Previous studies have shown that a downstream adaptor for Toll-like receptors (TLRs), myeloid differentiation primary response 88 (MyD88), plays a role in UVB-induced DNA damage and immunosuppression. [...] Read more.
Ultraviolet B (UVB) radiation triggers DNA damage and immune suppression, establishing conditions favorable for skin carcinogenesis. Previous studies have shown that a downstream adaptor for Toll-like receptors (TLRs), myeloid differentiation primary response 88 (MyD88), plays a role in UVB-induced DNA damage and immunosuppression. However, specific mechanisms for the effects on dendritic cells and T cells remain poorly understood. The objective of this study is to determine the role of MyD88 and TIR-domain-containing adaptor inducing interferon-β (TRIF), another key TLR downstream adaptor, in UVB-induced suppression of dendritic cell activity and T cell function. MyD88−/−, Trif−/−, and wild-type (WT) mice were evaluated for UVB-induced effects on dendritic cell, T cells, and contact hypersensitivity responses in skin. MyD88−/− mice exhibited significant resistance to UVB-induced immune suppression, compared to Trif−/− mice and wild-type controls. The MyD88 deficiency significantly reduced UVB-induced Treg cells that were CD4+CD25+Foxp3+ and produced interleukin (IL)-10. Moreover, it significantly inhibited the UVB-induced suppression of IL-12/IL-23 producing CD11c+ dendritic cells. Further experiments confirmed that MyD88 conditional knockout (MyD88fl/flXCD11c.Cre) mice were protected against UVB-induced immune suppression. Dendritic cells from MyD88 genomic or conditional knockout mice were resistant to UVB-induced reduction of major histocompatibility complex (MHC) class II antigens. These findings show that MyD88 plays a key role in UVB-induced immune suppression. The deficiency in the MyD88 gene inhibits UVB-induced suppression of CD11c+ dendritic cell (DC) activity and reduces UVB-induced development of Treg cells. Our studies demonstrate a new mechanism for MyD88-mediated regulation of UVB-induced immune suppression. Full article
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