Abstract
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.
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