ArticleJournal of immunology (Baltimore, Md. : 1950)2014
B cell differentiation is associated with reprogramming the CCCTC binding factor-dependent chromatin architecture of the murine MHC class II locus.
Article in Journal of immunology (Baltimore, Md. : 1950), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
18 citing papers in PubMed, 28 citations in OpenAlex.
- Selective control of HLA-DRB1 and HLA-DQA1 transcription through DR/DQ super enhancer microelements.Cell reports · 2026Article
- The Role of Dynamic DNA Methylation in Liver Transplant Rejection in Children.Transplantation direct · 2022Article
- H3K27me3 Demethylase UTX Restrains Plasma Cell Formation.Journal of immunology (Baltimore, Md. : 1950) · 2022Article
- Epigenomic priming of immune genes implicates oligodendroglia in multiple sclerosis susceptibility.Neuron · 2022Article
- Epigenetic gene regulation in plasma cells.Immunological reviews · 2021Review
- The Murine MHC Class II Super EnhancerJournal of immunology (Baltimore, Md. : 1950) · 2021Article
- Roadmap to a plasma cell: Epigenetic and transcriptional cues that guide B cell differentiation.Immunological reviews · 2021Review
- A super enhancer controls expression and chromatin architecture within the MHC class II locus.The Journal of experimental medicine · 2020Article
- Epigenetic Priming in Immunodeficiencies.Frontiers in cell and developmental biology · 2019Review
- The Histone Demethylase LSD1 Regulates B Cell Proliferation and Plasmablast Differentiation.Journal of immunology (Baltimore, Md. : 1950) · 2018Article
- Plasma cell differentiation is controlled by multiple cell division-coupled epigenetic programs.Nature communications · 2018Article
- Developing in 3D: the role of CTCF in cell differentiation.Development (Cambridge, England) · 2018Review
- EZH2 Represses the B Cell Transcriptional Program and Regulates Antibody-Secreting Cell Metabolism and Antibody Production.Journal of immunology (Baltimore, Md. : 1950) · 2018Article
- Article
- ChIP-seq analysis of genomic binding regions of five major transcription factors highlights a central role for ZIC2 in the mouse epiblast stem cell gene regulatory network.Development (Cambridge, England) · 2017Article
- Regions of very low H3K27me3 partition the Drosophila genome into topological domains.PloS one · 2017Article
- Genome-wide CIITA-binding profile identifies sequence preferences that dictate function versus recruitment.Nucleic acids research · 2015Article
- Common distal elements orchestrate CIITA isoform-specific expression in multiple cell types.Genes and immunity · 2014Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The transcriptional insulator CCCTC binding factor (CTCF) was shown previously to be critical for human MHC class II (MHC-II) gene expression. Whether the mechanisms used by CTCF in humans were similar to that of the mouse and whether the three-dimensional chromatin architecture created was specific to B cells were not defined. Genome-wide CTCF occupancy was defined for murine B cells and LPS-derived plasmablasts by chromatin immunoprecipitation sequencing. Fifteen CTCF sites within the murine MHC-II locus were associated with high CTCF binding in B cells. Only one-third of these sites displayed significant CTCF occupancy in plasmablasts. CTCF was required for maximal MHC-II gene expression in mouse B cells. In B cells, a subset of the CTCF regions interacted with each other, creating a three-dimensional architecture for the locus. Additional interactions occurred between MHC-II promoters and the CTCF sites. In contrast, a novel configuration occurred in plasma cells, which do not express MHC-II genes. Ectopic CIITA expression in plasma cells to induce MHC-II expression resulted in high levels of MHC-II proteins, but did not alter the plasma cell architecture completely. These data suggest that reorganizing the three-dimensional chromatin architecture is an epigenetic mechanism that accompanies the silencing of MHC-II genes as part of the cell fate commitment of plasma cells.
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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.