UV immunosuppression and cutaneous malignancies

Paul C Jou, Tom S. McCormick, Elma D. Baron

Research output: Contribution to journalReview articlepeer-review

4 Scopus citations

Abstract

Skin cancer is the most common cancer in the USA with ultraviolet radiation (UVR) exposure being the major environmental risk factor. The mechanism by which UVR causes cancer is not yet clear but involves direct and indirect DNA damage, as well as local and systemic immunosuppression leading to a tumorigenic environment. At the cellular level, dermal dendritic cells, Langerhans cells, skin-infiltrating monocyte/macrophages, T lymphocytes, chemokines and cytokines participate. Dermal dendritic cells are recognized as the main antigen presenting cell of the skin. UV-induced skin-infiltrating monocytes/macrophages may be a source for these dermal dendritic cells. Langerhans cells serve an immunosuppressive role and activate regulatory T cells upon UVR damage. CD4 +CD25+ regulatory T lymphocytes, upon activation by UV damage, suppress effector T lymphocyte proliferation, maturation and function, leading to decreased contact hypersensitivity responses. IL-12, a cytokine suppressed by UVR, is involved in DNA repair and is associated with decreased UV-induced immunosuppression, while IL-10, which is secreted in response to UVR, increases immunosuppression. This article will focus on current research into the mechanism of UV immunosuppression and its impact on skin cancers.

Original languageEnglish (US)
Pages (from-to)61-74
Number of pages14
JournalExpert Review of Dermatology
Volume6
Issue number1
DOIs
StatePublished - Feb 1 2011

Keywords

  • DNA damage
  • IL-10
  • IL-12
  • Langerhans cell
  • UV immunosuppression
  • basal cell carcinoma
  • dermal dendritic cell
  • melanoma
  • monocytes
  • regulatory T lymphocyte
  • skin cancer
  • squamous cell carcinoma

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