Glucocorticoid resistance is a dominant trait in hybrids between cytolytic T-lymphocyte lines and AKR thymomas.
By screening several cytolytic T-lymphocyte lines, AKR thymomas, and CTL X AKR thymoma hybrids from two different crosses for their sensitivity to the glucocorticoid (GC) analog dexamethasone (dex), we have found that CTL lines and cytolytically active, IL-2-dependent (CTL-like) hybrids are resistant to the cytostatic or cytolytic effects of dex; AKR thymomas and thymoma-like hybrids (cytolytically inactive, IL-2-independent), however, are sensitive to these effects of the drug. The GC resistance behaves like a dominant trait in these crosses. Although they are resistant to GC, the CTL lines and the CTL-like hybrids do contain functional hormone receptors and macrophage-activating factor (MAF) release by the CTL lines and CTL-like hybrids is inhibited by dex.
D000818:Animals; D002460:Cell Line; D003602:Cytotoxicity, Immunologic; D003907:Dexamethasone / Q000494:pharmacology*; D005799:Genes, Dominant; D014644:Genetic Variation; D006822:Hybrid Cells / Q000166:cytology* / Q000187:drug effects / Q000276:immunology; D008223:Lymphoma / Q000473:pathology; D051379:Mice; D008806:Mice, Inbred AKR; D008815:Mice, Inbred Strains; D013045:Species Specificity; D013602:T-Lymphocytes, Cytotoxic / Q000166:cytology* / Q000276:immunology; D013945:Thymoma / Q000473:pathology*; D013953:Thymus Neoplasms / Q000473:pathology*
D003907:Dexamethasone