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Figure 19.27 A. Time course for development of primary skin cancers and the susceptibility to the growth of transplanted skin cancers in C3H mice continuously exposed three times per week to UVB radiation. B. The percentage susceptibility of mice treated for 12 weeks (3 times per week) with UVB radiation to the growth of transplants of UV-induced neoplasms of the skin. (Adapted from Kripke, 1986, with permission of the author and publisher.)

Figure 19.27 A. Time course for development of primary skin cancers and the susceptibility to the growth of transplanted skin cancers in C3H mice continuously exposed three times per week to UVB radiation. B. The percentage susceptibility of mice treated for 12 weeks (3 times per week) with UVB radiation to the growth of transplants of UV-induced neoplasms of the skin. (Adapted from Kripke, 1986, with permission of the author and publisher.)

epidermoid carcinomas to the immune system, with subsequent rejection of the transplant in the case of the UV-induced carcinomas.

Ultraviolet-Mediated Immunosuppression

Since the transplantation of UV-induced epidermal carcinomas in mice could be accomplished virtually anywhere in the organism, it was clear that the effects of UVB irradiation were not simply local, as suggested by the failure of contact hypersensitivity only in regions of UV radiation. It now appears that there are several mechanisms for such generalized immunosuppression by UV radiation. The first of these is the fact that suppressor T cells that are specific for the UV radiation-induced neoplasms (Trial and McIntyre, 1990) have been induced in the organism as a result of UV radiation. This may be because a different population of antigen-presenting cells in =j the skin, relatively nonsusceptible to UVB irradiation, can act as antigen-presenting cells for suppressor T lymphocytes that likely express the y8 T cell receptor (see below) (cf. Meunier, 1999). In addition, there is evidence that immunosuppression by UV radiation of the skin is mediated by the UV-induced formation of the abnormal cis isomer of urocanic acid from the product of the action of histidine ammonia-lyase in the skin, which is the trans isomer. A diagram of

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