Lack of correlation between UV‐induced enhancement of melanoma development and local suppression of contact hypersensitivity

Abstract

Injection of melanoma cells into the UV-irradiated ear skin of syngeneic mice results in an increased incidence of melanomas compared with that in nonirradiated ear skin. This effect of UV is localized to the site of irradiation and appears to be immunologically mediated. In these studies we test the hypothesis that the effect of UV irradiation on melanoma development is related to its ability to alter epidermal Langerhans cells and impair the induction of contact hypersensitivity. A regimen of UV irradiation that altered epidermal immune cells and interfered with the generation of contact hypersensitivity was tested for its ability to increase the incidence of melanoma. Conversely, the ear skin of C3H mice treated with a regimen of UV radiation that enhanced melanoma development was examined for the number of appearance of ATPase+ and Thy-1+ dendritic epidermal cells and tested for the ability to initiate a contact hypersensitivity response. No correlation between these effects of UV irradiation could be detected. Furthermore, implantation of melanoma cells into UV-irradiated ear skin resulted in the generation of systemic immunity against subsequent tumor challenge. Therefore, we conclude that the ability of UV irradiation to modify melanoma development is unrelated to its effects on the afferent arm of the contact hypersensitivity response and that enhanced melanoma development is not due to an impairment in the induction of tumor immunity.

Effects of low‐dose ultraviolet radiation on in vivo human cutaneous recall responses

“…One report suggests that UVB irradiation promotes tumour outgrowth and tolerance to melanoma antigens in mice by suppressing the local effector mechanisms central in CHS to recall antigens, such as reduced numbers and activity of local CD8 + lymphocytes 30 . In contrast, UV suppression of afferent immune responses appeared unrelated to the increased tumour growth observed after UV exposure 31 . Enhancement of melanoma growth was unrelated to the erythemal effects of UV irradiation 32 .…”

Preservation of the Delayed-Type Hypersensitivity Response to Alloantigen by Xyloglucans or Oligogalacturonide does not Correlate with the Capacity to Reject Ultraviolet-Induced Skin Tumors in Mice

“…Both CHS and DTH responses are delayed-in-time and are T cell-mediated, although CHS immune responses are generally thought to be a subset of DTH immunity. Donawho et al (1992) showed that suppression of DTH responses to protein antigens but not CHS to hapten was important in UV enhanced outgrowth of melanoma. Similarly, Steerenberg et al (1997) were unable to correlate protection of CHS immune responses to picryl chloride and UV carcinogenesis, suggesting a dissociation between CHS and tumor immunity; however, the conditions used by these authors would also suppress DTH immunity to protein antigens.…”