Enhanced tumor growth in UV-irradiated skin is associated with an influx of inflammatory cells into the epidermis

UV radiation causes a number of cellular changes within the skin which play a role in tumor outgrowth, including immunosuppression and production of g rowth-enhancing cytokines, Both of these enable tumors to grow but their re lative importance in carcinogenesis is poorly defined. In this study, C3H/H eN mice were exposed to a single inflammatory dose of 410 mJ/cm(2) UVB radi ation (plus 100 mJ/cm2 UVA radiation) followed by the inoculation of a regr essor squamous cell carcinoma into or the painting of oxazolone onto the tr eated skin. Tumors transplanted 2 or 3 but not 4 days after irradiation had a significantly higher growth rate than tumors inoculated into unirradiate d control mice. In contrast, mice failed to respond to hapten when it was a pplied 2, 3 or 4 days after irradiation, Cytofluorimetric analysis demonstr ated that the number of F4/80(+) Langerhans cells was not significantly red uced until 4 days after irradiation, while the number of dendritic epiderma l T cells was significantly lower at all time points observed after UV-irra diation, Furthermore, a large cellular infiltration of CD11b(+), Gr-1(+), C D45(+) MHC class II+ and CD45(+) MHC class II- cells into the epidermis was observed 2 and 3 days after irradiation, which corresponded with the enhan ced tumor growth. To a lesser extent tumor growth was also associated with CD45(+) MHC class II+ cells, possibly the previously described UV-induced m acrophage, In contrast, suppression of contact hypersensitivity corresponde d with the reduction in dendritic epidermal T cells but not with other cell changes, The results suggest that, in this model, where immunosuppression did not appear to be responsible for enhanced tumor growth, inflammatory in filtrates may contribute to the promotion of skin tumor growth within UV-ir radiated skin.