Tumor-Directed Cellular Immunity in Malignant Melanoma and the Antigens That Evoke It

Cochran, Alistair J.

doi:10.1007/978-1-4684-4079-9_5

Cited by 1 publication

(1 citation statement)

References 33 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…One possible explanation for this phenomenon is that UV irradiation interferes with the ability of the skin to initiate immune responses and thereby decreases host resistance to the development of antigenic tumors. This is an attractive hypothesis because the murine melanomas, like human melanomas (4)(5)(6), are quite immunogenic (7), Also, UVR is known to reduce the number and alter the morphology and function of epidermal Langerhans cells (8,9) and to interfere with the afferent arm of the immune response to contact sensitizers (9)(10)(11)(12) and Herpes simplex virus (HSV) (13), Applying a contact sensitizer or HSV to UV-irradialed murine skin induces suppressor T lymphocytes instead of a normal contact or delayed-type hypersensitivity (CHS, DTH) response (10,14),…”

Section: Introductionmentioning

confidence: 99%

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

Donawho

Kripke

1992

Experimental Dermatology

View full text Add to dashboard Cite

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.

show abstract