Crosstalk Among UV‐Induced Inflammatory Mediators, DNA Damage and Epigenetic Regulators Facilitates Suppression of the Immune System
Open accessAbstract
The suppression of the immune system by overexposure to ultraviolet (UV) radiation has been implicated in the initiation and progression of photocarcinogenesis. Numerous changes occur in the skin on UVB exposure, including the generation of inflammatory mediators, DNA damage, epigenetic modifications, and migration and functional alterations in the antigen‐presenting dendritic cells. Although each of these alterations can elicit a cascade of events that have the potential to modulate immune sensitivity alone, there is emerging evidence that there is considerable crosstalk between these cascades. The development of an understanding of UV‐induced changes in the skin that culminate in UV‐induced immunosuppression, which has been implicated in the risk of nonmelanoma skin cancer, as a network of events has implications for the development of more effective chemopreventive strategies. In the current review article, we discuss the evidence of interactions between the various molecular targets and signaling mechanisms associated with UV‐induced immunosuppression.
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The DNA damage response is a potent activator of inflammatory responses.
“The DDR is a potent activator of inflammatory responses.”
From The central role of DNA damage in the ageing process (2021) · cites this paper as [90]
Rapid repair of dipyrimidine photoproducts is expected to greatly minimize UV-induced immune suppression because the duration of unrepaired CPDs in genomic DNA is a primary signal for initiating this suppression.
“This rapid repair of dipyrimidine photoproducts is also expected to greatly minimize UV-induced immune suppression since one of the primary signals for initiating this suppression is the duration of unrepaired CPDs in genomic DNAs25,37–39.”
From Modulation of UVB-induced Carcinogenesis by Activation of Alternative DNA Repair Pathways (2018) · cites this paper as [37]
Solar UV exposure acts as a systemic immunosuppressant, compromising an individual's immune response with mechanistic implications for photocarcinogenesis.
“Contributing to the adverse effects of solar UV exposure is its known action as a systemic immunosuppressant, compromising an individual’s immune response with mechanistic implications for photocarcinogenesis (13).”
From Hypochlorous Acid: From Innate Immune Factor and Environmental Toxicant to Chemopreventive Agent Targeting Solar UV-Induced Skin Cancer (2022) · cites this paper as [13]
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- Authors
- Prasad, R., & Katiyar, S. K.
- Affiliations
- University of Alabama at Birmingham (US)
- Corresponding author
- Katiyar, Santosh K.
- Venue
- Photochemistry and Photobiology
- Publisher
- Wiley
- Published
- 2017-02-06
- Volume
- 93
- Issue
- 4
- Pages
- 930-936
- ISSN
- 0031-8655 (ISSN-L)
- 1751-1097
- PMC
- PMC5466507
- OpenAlex
- W2559933290
- Cited by
- 60
- References
- 63
- Citations by year
- 2026: 4 · 2025: 6 · 2024: 9 · 2023: 2 · 2022: 8 · 2021: 9 · 2019: 7 · 2018: 9 · 2017: 6
- FWCI
- 1.05
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Photochemistry and Photobiology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (CA140197, AT002536)
- Topics
- Health Sciences › Medicine › Dermatology › Skin Protection and Aging
- Health Sciences › Medicine › Epidemiology › Nonmelanoma Skin Cancer Studies
- Life Sciences › Immunology and Microbiology › Immunology › Psoriasis: Treatment and Pathogenesis
- Keywords
- ultraviolet radiation, UV-B radiation, immunosuppression, photocarcinogenesis, non-melanoma skin cancer, inflammatory mediators, DNA damage, epigenetic modifications, dendritic cells, antigen presentation, chemoprevention, skin
- MeSH terms
- Animals, DNA Damage, Humans, Immune System, Neoplasms, Radiation-Induced, Skin, Skin Neoplasms, Sunlight, Ultraviolet Rays, Inflammation Mediators, Epigenesis, Genetic
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