Induction of MHC Class I Expression by the MHC Class II Transactivator CIITA

• Published in: Immunity (Cambridge, Mass.) Mass.), 1997-05, Vol.6 (5), p.591-600
• Main Authors: Martin, Brian K, Chin, Keh-Chuang, Olsen, John C, Skinner, Cheryl A, Dey, Anup, Ozato, Keiko, Ting, Jenny P.-Y
• Format: Article
• Language: English
• Subjects: Breast Neoplasms; Carcinoma; Chloramphenicol O-Acetyltransferase - genetics; Electrophoresis, Polyacrylamide Gel; Gene Expression Regulation, Neoplastic; Genes, MHC Class II - physiology; Genes, Reporter; Histocompatibility Antigens Class I - biosynthesis; Histocompatibility Antigens Class I - genetics; Humans; Leukemia, Myelogenous, Chronic, BCR-ABL Positive; Mutation; Nuclear Proteins; Promoter Regions, Genetic; Trans-Activators - genetics; Trans-Activators - physiology; Transcriptional Activation; Tumor Cells, Cultured
• ISSN: 1074-7613; 1097-4180
• DOI: 10.1016/S1074-7613(00)80347-7

Major histocompatibility complex (MHC) class I–deficient cell lines were used to demonstrate that the MHC class II transactivator ( CIITA) can induce surface expression of MHC class I molecules. CIITA induces the promoter of MHC class I heavy chain genes. The site α DNA element is the target for CIITA-induced transactivation of class I. In addition, interferon-γ (IFNγ)–induced MHC class I expression also requires an intact site α. The G3A cell line, which is defective in CIITA induction, does not induce MHC class I antigen and promoter in response to IFNγ. Trans-dominant–negative forms of CIITA reduce class I MHC promoter function and surface antigen expression. Collectively, these data argue that CIITA has a role in class I MHC gene induction.