Loss of MHC class II inducibility in hyperplastic tissue in Rb-defective mice

• Published in: Cancer letters Vol. 171; no. 2; pp. 209 - 214
• Main Authors: Eason, Donna D, Coppola, Domenico, Livingston, Sandra, Shepherd, Alexander T, Blanck, George
• Format: Journal Article
• Language: English
• Published: Shannon Elsevier Ireland Ltd 10-10-2001; Elsevier
• Subjects: Animals; Biological and medical sciences; Carcinogenesis, carcinogens and anticarcinogens; Female; Gene Expression Regulation; General aspects; Genes, MHC Class II; Genes, Retinoblastoma - genetics; Histocompatibility Antigens Class II - biosynthesis; Histocompatibility Antigens Class II - genetics; Hyperplasia - immunology; Hyperplasia - metabolism; Immunohistochemistry; Interferon-gamma - pharmacology; Male; Medical sciences; MHC; Mice; Mice, Inbred C57BL; Mice, Knockout; Precancerous Conditions - genetics; Precancerous Conditions - immunology; Precancerous Conditions - metabolism; Rb gene; Retinoblastoma Protein - deficiency; Retinoblastoma Protein - physiology; Tumors; Rb; IL-8, interlukin 8; Rb, retinoblastoma gene; TIL, tumor infiltrating lymphocyte; MHC; MEFs, mouse embryonic fibroblasts; IFN-γ, interferon-gamma; MHC class II, major histocompatibility complex class II; Tumors; Retinoblastoma gene; Hyperplasia; Major histocompatibility system; Rodentia; Class II histocompatibility antigen; Cytokine; Tumorous infiltration; Tumoral marker; Malignant tumor; Gene expression; Vertebrata; Mammalia; Mouse; Animal; Lymphocyte; Gamma interferon
• ISSN: 0304-3835; 1872-7980
• DOI: 10.1016/S0304-3835(01)00603-6

Retinoblastoma gene (Rb) defects occur frequently in human tumors. Studies of Rb-defective human tumor cell lines and Rb−/− murine embryonic fibroblasts demonstrate that Rb is required for interferon-gamma (IFN-γ) induced major histocompatibility complex (MHC) class II expression. MHC class II expressing tumors generate anti-tumor immune responses associated with tumor-specific infiltrating lymphocytes. The role of Rb in IFN-γ induced MHC class II expression on an endogenous tumor was examined by immunohistochemical staining for IAβ and Rb on tissues from Rb+/− mice. MHC class II IAβ is not induced by IFN-γ in Rb-deficient neoplastic cells, but remains inducible in related normal tissue.