Tags

Type your tag names separated by a space and hit enter

Regulation of MHC class II expression in glioma cells by class II transactivator (CIITA).
Glia. 2004 Mar; 45(4):392-405.GLIA

Abstract

We first classified 12 malignant glioma cell lines into three different groups (types 1-3) with respect to major histocompatibility complex (MHC) class II expression and analyzed each group based on the different expression status of the class II transactivator (CIITA) gene. Glioma type 1 (2 of 12) showed constitutive expression of all class II molecules that might be mediated by activation of B cell-specific CIITA promoter III. Glioma type 2 represented the major phenotype (66.7 %) of malignant glioma cell lines, and MHC class II expression was induced by interferon-gamma (IFN-gamma) in this phenotype. Analysis of glioma tissue samples revealed that CIITA promoter IV was detected in 9 of 11 patients (81.8%); however, promoter III was only in two (18.2%). Moreover, cultured glioma cells obtained from a fresh tumor sample upregulated expression of CIITA and class II molecules in the presence of IFN-gamma, strongly suggesting that glioma type 2 might be predominant in glioma tissues. Glioma type 3 (2 of 12) showed CIITA transcripts but loss of MHC class II expression even in the presence of IFN-gamma. In addition, we determined that the constitutive MHC class II expression in the glioma cell lines (type 1) was the result of transcriptional activation of the CIITA gene. This phenomenon was mediated by global histone acetylation over 6 kb upstream from the transcriptional start site of CIITA promoter III. Moreover, stable transfection of CIITA promoter IV as well as promoter III into MHC class II inducible cell lines restored the constitutive expression of all class II molecules. These studies lay the foundation to understand the molecular basis for the expression of class II molecules in gliomas.

Authors+Show Affiliations

Department of Pathology, Sapporo Medical University School of Medicine, Sapporo, Japan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

14966870

Citation

Takamura, Yukio, et al. "Regulation of MHC Class II Expression in Glioma Cells By Class II Transactivator (CIITA)." Glia, vol. 45, no. 4, 2004, pp. 392-405.
Takamura Y, Ikeda H, Kanaseki T, et al. Regulation of MHC class II expression in glioma cells by class II transactivator (CIITA). Glia. 2004;45(4):392-405.
Takamura, Y., Ikeda, H., Kanaseki, T., Toyota, M., Tokino, T., Imai, K., Houkin, K., & Sato, N. (2004). Regulation of MHC class II expression in glioma cells by class II transactivator (CIITA). Glia, 45(4), 392-405.
Takamura Y, et al. Regulation of MHC Class II Expression in Glioma Cells By Class II Transactivator (CIITA). Glia. 2004;45(4):392-405. PubMed PMID: 14966870.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Regulation of MHC class II expression in glioma cells by class II transactivator (CIITA). AU - Takamura,Yukio, AU - Ikeda,Hideyuki, AU - Kanaseki,Takayuki, AU - Toyota,Minoru, AU - Tokino,Takashi, AU - Imai,Kohzoh, AU - Houkin,Kiyohiro, AU - Sato,Noriyuki, PY - 2004/2/18/pubmed PY - 2004/4/15/medline PY - 2004/2/18/entrez SP - 392 EP - 405 JF - Glia JO - Glia VL - 45 IS - 4 N2 - We first classified 12 malignant glioma cell lines into three different groups (types 1-3) with respect to major histocompatibility complex (MHC) class II expression and analyzed each group based on the different expression status of the class II transactivator (CIITA) gene. Glioma type 1 (2 of 12) showed constitutive expression of all class II molecules that might be mediated by activation of B cell-specific CIITA promoter III. Glioma type 2 represented the major phenotype (66.7 %) of malignant glioma cell lines, and MHC class II expression was induced by interferon-gamma (IFN-gamma) in this phenotype. Analysis of glioma tissue samples revealed that CIITA promoter IV was detected in 9 of 11 patients (81.8%); however, promoter III was only in two (18.2%). Moreover, cultured glioma cells obtained from a fresh tumor sample upregulated expression of CIITA and class II molecules in the presence of IFN-gamma, strongly suggesting that glioma type 2 might be predominant in glioma tissues. Glioma type 3 (2 of 12) showed CIITA transcripts but loss of MHC class II expression even in the presence of IFN-gamma. In addition, we determined that the constitutive MHC class II expression in the glioma cell lines (type 1) was the result of transcriptional activation of the CIITA gene. This phenomenon was mediated by global histone acetylation over 6 kb upstream from the transcriptional start site of CIITA promoter III. Moreover, stable transfection of CIITA promoter IV as well as promoter III into MHC class II inducible cell lines restored the constitutive expression of all class II molecules. These studies lay the foundation to understand the molecular basis for the expression of class II molecules in gliomas. SN - 0894-1491 UR - https://www.unboundmedicine.com/medline/citation/14966870/Regulation_of_MHC_class_II_expression_in_glioma_cells_by_class_II_transactivator__CIITA__ L2 - https://doi.org/10.1002/glia.10343 DB - PRIME DP - Unbound Medicine ER -