Affiliations 

  • 1 Cellular Photoimmunology Group; Discipline of Infectious Diseases and Immunology; Sydney Medical School; University of Sydney; Sydney, NSW Australia ; Department of Dermatology; Royal Prince Alfred Hospital; Camperdown, NSW Australia ; Discipline of Dermatology at The Bosch Institute; Sydney Medical School; University of Sydney; Sydney, NSW Australia
  • 2 Cellular Photoimmunology Group; Discipline of Infectious Diseases and Immunology; Sydney Medical School; University of Sydney; Sydney, NSW Australia ; Department of Dermatology; Royal Prince Alfred Hospital; Camperdown, NSW Australia ; Discipline of Dermatology at The Bosch Institute; Sydney Medical School; University of Sydney; Sydney, NSW Australia ; Faculty of Medicine and Health Sciences; Universiti Putra Malaysia; Malaysia
Oncoimmunology, 2014 Jan 01;3(1):e27562.
PMID: 24744978

Abstract

Sunlight causes skin cancer by directly damaging DNA as well as by suppressing antitumor immune responses. A major mechanism whereby sunlight exerts immunosuppressive effects is by modulating the migration of chemokine (C-X-C motif) receptor 4 (CXCR4)-expressing dermal mast cells into and away from the skin. We have demonstrated the importance of this by showing that the systemic administration of the CXCR4 antagonist AMD3100 prevents sunlight-induced immunosuppression as well as the consequent carcinogenic response. Our results highlight the therapeutic potential of antagonizing CXCR4 signaling, especially in individuals who are at high risk of developing skin cancer.

* Title and MeSH Headings from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.