ArticleInternational immunology2008
Methylation of CIITA promoter IV causes loss of HLA-II inducibility by IFN-gamma in promyelocytic cells.
Article in International immunology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- Epigenetic induction of adaptive immune response in multiple myeloma: sequential azacitidine and lenalidomide generate cancer testis antigen-specific cellular immunity.British journal of haematology · 2012Trial
- CLEVER-1 targeting antibody, bexmarilimab, supports HLA-DR expression and alters ex vivo responsiveness to azacitidine and venetoclax in myeloid malignancies.Scientific reports · 2025Article
- Beyond gluten: the multifaceted regulation of MHC class II in celiac disease pathogenesis.Gastroenterology and hepatology from bed to bench · 2025Review
- Network and pathway-based analysis of genes associated with esophageal squamous cell carcinoma.Annals of translational medicine · 2023Article
- Distinct Molecular Mechanisms of Altered HLA Class II Expression in Malignant Melanoma.Cancers · 2021Article
- Article
- Epigenetic modification and preliminary investigation of the mechanism of the immune evasion of HL-60 cells.Molecular medicine reports · 2015Article
- HLA-DRB1 and HLA-DQB1 methylation changes promote the occurrence and progression of Kazakh ESCC.Epigenetics · 2014Article
- Expression regulation of major histocompatibility complex class I and class II encoding genes.Frontiers in immunology · 2011Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The human promyelocytic cell line THP-1 expresses high level of HLA class II (HLA-II) molecules after IFN-gamma treatment. Here, we report a variant of THP-1 that does not express HLA-II after IFN-gamma. The variant's HLA-II phenotype is constant over time in culture and it is not related to a defective IFN-gamma-signalling pathway. Transfection of CIITA, the HLA-II transcriptional activator, under the control of a cytomegalovirus promoter rescues high level of HLA-DR surface expression in the variant indicating that the biosynthetic block resides in the expression of CIITA and not in the CIITA-dependent transactivation of the HLA-II promoters. Treatment of the variant with 5-azacytidine (5-aza), which inhibits CpG methylation, restores inducibility of HLA-II by IFN-gamma both at transcriptional and phenotypic level and antigen presenting and processing function of the variant. DNA studies demonstrate that the molecular defect of the THP-1 variant originates from the methylation of the CIITA promoter IV. Furthermore, treatment with 5-aza produces a substantial demethylation of CIITA promoter IV and a significant increase of IFN-gamma-dependent HLA-II expression in another myelomonocytic cell line, U937. Therefore hyper-methylation of CIITA promoter IV may be a relevant mechanism of epigenetic control preventing HLA-II IFN-gamma inducibility in the myelomonocytic cell lineage.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.