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ABSTRACT
The object of this paper is to review, firstly, the mechanisms that are involved in the induction of dysplastic changes in the epidermis by sunlight and, secondly, the effect of UV light on the immune response to these changes. The role of pigmentation in preventing changes in the immune response and the relative importance of the immune response compared to the presence of melanin in black skin are discussed.
Impairment of the immune response to dysplastic cells by HIV infection may also be a factor in increasing predisposition to epidermal cancer
The causes of differences in the clinical changes of photodermatoses in white and black skin are also considered.
Melanin in the epidermis is the primary protective mechanism against the effect of UV radiation and accounts for the very small incidence of carcinoma in black skin.
In Albinism there is an increased incidence of epidermal cancer. UVB rays of the sun are responsible for DNA damage and mutations that result in dysplastic changes in the epidermis leading to cancerous lesions. UV light also causes alteration of the immune responses occurring in the skin, as shown by diminished contact hypersensitivity and delayed immune response. This is associated with the transformation of trans-urocanic acid (Trans UCA) to cis-urocanic acid (Cis UCA). Other immunological changes occur including increases in tnf a , CD10 T cells and IL10.
There is a relative diminution in cytotoxic CD8 Tcells and there is also evidence for diminished CD4 Tcell activity linked to changes in antigen recognition by Antigen Presenting Cells (APCs). It may be that, as well as UVLight, HIV infection leads to an increased susceptibility to skin cancer by diminishing the CD4 T cell response.
As a result the dysplastic cells escape the normal immunological response leading to proliferation of cancer cells. |
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