RB and A novel E2F-1 binding protein in MHC class II deficient B-cell lines and normal IFN-γ induction of the class II transactivator ciita in class II non-inducible RB-defective tumor lines

✍ Scribed by Michael E. Tschickardt; Yanmei Lu; Mark Jacim; G. de Wayne Ussery; Viktor Steimle; Bernard Mach; George Blanck

• Publisher: John Wiley and Sons
• Year: 1995
• Tongue: French
• Weight: 611 KB
• Volume: 62
• Category: Article
• ISSN: 0020-7136
• DOI: 10.1002/ijc.2910620417

✦ Synopsis

The major histocompatibility (MHC) class II genes encode cell surface proteins that bind antigenic peptide for presentation to T-cells. The class II proteins are expressed constitutively on B-cells and EBV-transformed B-cells, and are inducible by IFN-y on a wide variety of cell types. Retinoblastoma protein (RB) is a tumor suppressor and functions as a transcriptional repressor by binding and inactivating the transactivator E2F-I . RBdefective tumor lines are non-inducible for MHC class II by IFN-y, or very weakly inducible, but transfection of 2 different lines with RB expression vectors re-establishes or substantially enhances class II inducibility. Therefore, we examined the RB status of a series of B-cell mutants that are defective in class II expression, generated either in vitro or derived from Bare Lymphocyte Syndrome (BLS) patients. Nuclear matrix-bound RB was detectable in all cases, indicating that loss of RB is not responsible for decreased class II expression in these lines. A second E2F-I binding protein, most likely DP-I, was also apparantly normal in both class Il-positive and -negative B-cell lines. We also examined the IFN-y induction of CllTA in RB-defective lines. CllTA is a class II gene transactivator known to be defective in one form of BLS and to be required for the induction of MHC class II by IFN-y. CllTA mRNA is normally inducible by IFN-y in class II non-inducible, RB-defective lines, and in one line, re-expression of RB has no effect on CllTA mRNA induction levels. Thus, the block in MHC class II inducibility in RB-defective cells is not due to a block in CllTA inducibiliy -, ,