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This title is printed to order. This book may have been self-published. If so, we cannot guarantee the quality of the content. In the main most books will have gone through the editing process however some may not. We therefore suggest that you be aware of this before ordering this book. If in doubt check either the author or publisher’s details as we are unable to accept any returns unless they are faulty. Please contact us if you have any questions.
Ultraviolet radiation, a component of sunlight, has been recognized by photobiologists, dermatologists, and oculists as a potential hazard for human health because of its genotoxic, carcinogenic and immunotoxic properties. Its effects on human health include the induction of skin cancers, ocular damage and impairment of immunity to certain infections. A few decennia ago it was demonstrated that UV photons can affect the activity of the immune system through interactions with the skin. This means that UV not only changes normal cells into cancer cells but also permits the outgrowth of the UV -transformed cells by depressing the immune system. An intriguing question is what interactions between UV radiation and the skin initiates alterations in immune function in the exposed skin and systemically, i. e. in other places than the exposed skin. During the last 20 years many studies have been performed in order to investigate the immunosuppressive activities of UVB in laboratory animals and in human volunteers. In particular effects of UVB radiation on resistance to tumours and skin associated infections have been examined. In addition, effects of UVB radiation on immune parameters such as contact hypersensitivity and delayed-type hypersensitivity (both type IV hypersensitivity reactions), mixed lymphocyte reactions, mixed skin lymphocyte reactions, antigen presentation and numbers and function of Langerhans cells have been studied intensively. The antigenicity of murine tumours which are caused by UVB radiation was one of the first items to be investigated (Kripke, 1974).
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This title is printed to order. This book may have been self-published. If so, we cannot guarantee the quality of the content. In the main most books will have gone through the editing process however some may not. We therefore suggest that you be aware of this before ordering this book. If in doubt check either the author or publisher’s details as we are unable to accept any returns unless they are faulty. Please contact us if you have any questions.
Ultraviolet radiation, a component of sunlight, has been recognized by photobiologists, dermatologists, and oculists as a potential hazard for human health because of its genotoxic, carcinogenic and immunotoxic properties. Its effects on human health include the induction of skin cancers, ocular damage and impairment of immunity to certain infections. A few decennia ago it was demonstrated that UV photons can affect the activity of the immune system through interactions with the skin. This means that UV not only changes normal cells into cancer cells but also permits the outgrowth of the UV -transformed cells by depressing the immune system. An intriguing question is what interactions between UV radiation and the skin initiates alterations in immune function in the exposed skin and systemically, i. e. in other places than the exposed skin. During the last 20 years many studies have been performed in order to investigate the immunosuppressive activities of UVB in laboratory animals and in human volunteers. In particular effects of UVB radiation on resistance to tumours and skin associated infections have been examined. In addition, effects of UVB radiation on immune parameters such as contact hypersensitivity and delayed-type hypersensitivity (both type IV hypersensitivity reactions), mixed lymphocyte reactions, mixed skin lymphocyte reactions, antigen presentation and numbers and function of Langerhans cells have been studied intensively. The antigenicity of murine tumours which are caused by UVB radiation was one of the first items to be investigated (Kripke, 1974).