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Cited by 31Nonmelanoma Skin Cancer StudiesSkin Protection and AgingImmunotherapy and Immune Responses

Immune Response Associated with Nonmelanoma Skin Cancer

Strickland, Faith M., Kripke, Margaret L.·1997·Clinics in Plastic Surgery
DOI 10.1016/s0094-1298(20)32287-2
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Abstract

It is now clear that UV radiation causes nonmelanoma skin cancer in at least two ways: by causing permanent changes in the genetic code and by preventing immunologic recognition of mutant cells. These are interacting rather than separate mechanisms. Damage to DNA results in disregulation of cellular proliferation and initiates immune suppression by stimulating the production of suppressive cytokines. These cytokines contribute to the loss of immunosurveillance. Ultraviolet radiation has both local and systemic immunosuppressive effects. Locally, it depletes and alters antigen-presenting LC at the site of UV irradiation. Systemic suppression results when Ts cells are induced, by altered LC, by inflammatory macrophages that enter the skin following UV irradiation, or by the action of cytokines. Damage to DNA appears to be one of the triggering events in inducing systemic immunosuppression via the release of immunosuppressive cytokines and mediators. Immunologic approaches to treating skin cancers so far have concentrated on nonspecifically stimulating immune cells that infiltrate these tumors, but induction of specific immune responses against these tumors with antitumor vaccines has received little attention as yet. Preventive measures include sun avoidance and the use of sunscreens to prevent DNA damage by UV light. Future strategies may employ means to reverse UV-induced immunosuppression by using anti-inflammatory agents, biologicals that accelerate DNA repair or prevent the generation of immunosuppressive cytokines, and specific immunotherapy with tumor antigens. New approaches for studying the immunology of human skin cancers are needed to accelerate progress in this field.

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Crossref · 10.1016/s0094-1298(20)32287-2

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83 of 83 references verified0 citation errors · 0 not checkable

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  • 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 [38]

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Authors
Strickland, F. M., & Kripke, M. L.
Affiliations
The University of Texas MD Anderson Cancer Center (US)
ORCID
Strickland, Faith M.
Venue
Clinics in Plastic Surgery
Publisher
Elsevier BV
Published
1997-10
Volume
24
Issue
4
Pages
637-647
ISSN
0094-1298 (ISSN-L)
DOI
10.1016/s0094-1298(20)32287-2
OpenAlex
W2407759944
Cited by
31
References
83
Citations by year
2025: 1 · 2022: 1 · 2020: 1 · 2019: 1 · 2018: 2 · 2017: 1 · 2013: 2 · 2012: 2
FWCI
1.87
Type
journal article
Language
en
Open access
closed
Licence
Locations
  • Clinics in Plastic Surgery (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Epidemiology › Nonmelanoma Skin Cancer Studies
  • Health Sciences › Medicine › Dermatology › Skin Protection and Aging
  • Life Sciences › Immunology and Microbiology › Immunology › Immunotherapy and Immune Responses
Keywords
non-melanoma skin cancer, ultraviolet radiation, immunosuppression, immune surveillance, DNA damage, regulatory T cells, Langerhans cells, antigen presentation, macrophages, immunosuppressive cytokines, cancer vaccines, tumor-specific immunotherapy, sunscreen, sun avoidance, DNA repair, skin cancer prevention
MeSH terms
Animals, Antigen-Presenting Cells, Basal Cell Carcinoma, Carcinoma, Squamous Cell, Cell Movement, DNA Damage, Humans, Immune Tolerance, Skin, Skin Neoplasms, Ultraviolet Rays, Cytokines

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