title: Relationship between inducible H-2 expression and the immunogenicity of murine skin neoplasms. I. Evidence that the immunogenicity of ultraviolet radiation-chemically induced tumors is associated with their susceptibility to gamma-interferon-mediated enhancement of H-2Kk expression.
abstract: Our objective was to determine the relationship between major histocompatibility complex class I molecule expression and the tumorigenic properties of cutaneous neoplasms induced by ultraviolet radiation or chemical carcinogens. All tumors tested were found to express low constitutive levels of MHC class I molecules in vitro as determined by indirect immunofluorescence and flow cytometry. Those tumors capable of growth in UVR-exposed but not in normal recipients (regressors) were found to express enhanced levels of H-2Kk following incubation in the presence of gamma-IFN. In contrast, only one of the tumors that were capable of growth in normal recipients (progressors) exhibited more than moderate enhancement of H-2Kk expression in response to gamma-IFN. Analysis of tumor variants obtained by conversion of a UVR-induced regressor tumor to the progressor phenotype by passage through sublethally gamma-irradiated hosts, or the generation of regressor tumors by mutagen exposure of a benz [A] pyrene (BAP) induced progressor tumor, further supported the direct relationship between tumor immunogenicity in vivo and the capacity to elevate H-2Kk expression in response to gamma-IFN. No correlation existed between H-2Dk expression by the tumors and their transplantation phenotype. Furthermore, we failed to observe MHC class II expression by any of the tumors tested. Finally, the growth rate of a regressor tumor implanted into UVR-exposed hosts was significantly reduced if the tumor was pretreated with gamma-IFN in vitro prior to inoculation. This result suggests that UVR-exposed animals may be deficient in their ability to enhance the expression of MHC class I molecules on developing tumors. This alteration may, in part, account for the state of tumor susceptibility caused by UVR exposure.
authors.affiliation: Department of Pathology, University of Utah School of Medicine, Salt Lake City 84132.
authors.forename: D K
authors.initials: DK
authors.lastname: Burnham
authors.forename: C K
authors.initials: CK
authors.lastname: Mak
authors.forename: R J
authors.initials: RJ
authors.lastname: Webster
authors.forename: R A
authors.initials: RA
authors.lastname: Daynes
mesh_terms: D000818:Animals; D000954:Antigens, Surface / Q000235:genetics; D014644:Genetic Variation; D006183:H-2 Antigens / Q000276:immunology*; D015395:Histocompatibility Antigens Class I / Q000276:immunology; D007371:Interferon-gamma / Q000494:pharmacology*; D008285:Major Histocompatibility Complex; D051379:Mice; D008815:Mice, Inbred Strains; D009368:Neoplasm Transplantation; D009381:Neoplasms, Radiation-Induced / Q000235:genetics / Q000276:immunology*; D010641:Phenotype; D012878:Skin Neoplasms / Q000276:immunology*; D014466:Ultraviolet Rays
chemical_list: D000954:Antigens, Surface; D006183:H-2 Antigens; D015395:Histocompatibility Antigens Class I; D007371:Interferon-gamma