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Transcriptional down-regulation of major histocompatibility complex as a possible pathogenesis for Meniere's disease

ABSTRACT: Transcriptional down-regulation of major histocompatibility complex as a possible pathogenesis for Meniere's disease

PROVIDER: PRJNA836892 | ENA |

REPOSITORIES: ENA

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Transcriptional down-regulation of major histocompatibility complex as a possible pathogenesis for Meniere's disease

Project description:This study aimed to determine the underlying pathogenesis of Meniere's disease (MD) using transcriptome analysis

2022-05-11 | GSE202657 | GEO

Transcriptional Down-Regulation of Major Histocompatibility Complex as a Possible Pathogenesis for Meniere's Disease.

Project description:ObjectivesThis study aimed to determine the underlying pathogenesis of Meniere's disease (MD) using transcriptome analysis.MethodsTotal RNA was extracted from the peripheral blood mononuclear cells of 39 patients with MD and 39 controls. Through microarray analysis for nine patients and controls, the differentially expressed genes (DEGs) of those two groups were screened based on cut-off criteria (|fold changes| > 2.0 and adjusted p-value < 0.05). The functional enrichment analysis of DEGs was performed using Gene Ontology (GO).ResultsThere were 996 DEGs identified in the MD group: 415 were upregulated and 581 were downregulated. A functional enrichment analysis indicated that the downregulated DEGs were significantly enriched in terms related to immune system processes. Among them, 17 genes were enriched in terms for the major histocompatibility complex (MHC) protein complex, and the relative messenger RNA (mRNA) levels of three markedly downregulated DEGs [fold changes < -5: human leukocyte antigen (HLA)-DMA, HLA-DRB1, and HLA-DPB1] were significantly decreased in another 30 patients with MD compared with normal controls by quantitative reverse transcription-polymerase chain reaction (qRT-PCR). However, there were no correlations between the expression levels of these three genes and clinical data, such as age, onset age, time course, or hearing threshold.ConclusionsOur transcriptome analysis showed that the downregulated DEGs in MD were mainly associated with the immune system pathways including the MHC protein complex in MD. Remarkably, a breakdown in immunological tolerance mediated by MHC class II may contribute to the MD development, which has implications for targeted treatment.

| S-EPMC9339969 | biostudies-literature

DNA methylation changes at major histocompatibility complex in multiple sclerosis

Project description:DNA methylation changes at major histocompatibility complex in multiple sclerosis

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Kinetics of abacavir-induced remodelling of the Major Histocompatibility Complex class I peptide repertoire

Project description:Characterisation of the kinetics of abacavir-induced perturbation of the immunopeptidome of the Major Histocompatibility Complex (MHC) class I molecule HLA-B*57:01.

2021-05-11 | PXD024331 | Pride

Hypomethylation mediates genetic association with the major histocompatibility complex genes in Sjögren's syndrome

Project description:Hypomethylation mediates genetic association with the major histocompatibility complex genes in Sjögren's syndrome

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DNA methylation changes at major histocompatibility complex in multiple sclerosis

Project description:The major histocompatibility complex (MHC) region represents by far the strongest multiple sclerosis (MS) susceptibility loci. DNA methylation changes have been consistently detected at the MHC region in MS. However, understanding the full picture of epigenetic regulations of MHC in MS remains challenging, due in part to the limited coverage in the region by standard whole genome bisulfite sequencing or array-based methods. To fill this gap, we utilized a novel but validated MHC capture protocol with bisulfite sequencing and conducted a comprehensive analysis of MHC methylation landscapes in blood samples from 147 treatment naïve MS participants and 129 healthy controls. We identified 132 differentially methylated region (DMRs) within MHC regions and found they are significantly overlapped with MS risk variants. Integration of the MHC methylome to human leukocyte antigen (HLA) genetic data further indicate that the methylation changes are significantly associated with HLA genotypes. Using DNA methylation quantitative trait loci (mQTL) mapping and the causal inference test (CIT), we identified 643 cis-mQTL-DMRs paired associations including 71 DMRs possibly mediating causal relationships between 55 SNPs and MS risk.

2023-11-28 | GSE235106 | GEO

Transcription profiling of yeast expressing mouse major histocompatibility complex class I heavy chain H-2K(b)

Project description:To dissect the requirements of membrane protein degradation from the ER, we expressed the mouse major histocompatibility complex class I heavy chain H-2K(b) in yeast. Like other proteins degraded from the ER, unassembled H-2K(b) heavy chains are not transported to the Golgi but are degraded in a proteasome-dependent manner. The overexpression of H-2K(b) heavy chains induces the unfolded protein response (UPR). In yeast mutants unable to mount the UPR, H-2K(b) heavy chains are greatly stabilized. This defect in degradation is suppressed by the expression of the active form of Hac1p, the transcription factor that upregulates UPR-induced genes. These results indicate that induction of the UPR is required for the degradation of protein substrates from the ER.

2005-06-28 | E-SMDB-1576 | biostudies-arrayexpress

Genetic variants in Major Histocompatibility Complex-linked genes Associate with Pediatric Liver Transplant Rejection

Project description:Limited access to large samples and independent replication cohorts precludes genome-wide association (GWA) studies of rare but complex traits. To localize candidate genes in an on-going study utilizing family-based GWA, a novel exploratory analysis was first tested on 1,774 major histocompatibility complex single nucleotide polymorphisms (SNPs) in 240 DNA samples from 80 children with primary liver transplantation (LTx), and their biological parents. Genotyping was performed using the Illumina HumHap550k SNP BeadArray; the genotype calls for the 1813 SNPs in the MHC region are provided in the genotype_data.zip supplementary file linked to this series (see README file in the zip archive for more information). The Affymetrix Human Exon 1.0 ST array was used to measure differential splicing patterns in archived RNA isolated from 26 of 80 children for genes found near associated SNPs. This SuperSeries is composed of the SubSeries listed below.

2008-09-15 | GSE11361 | GEO

The CCR4-NOT complex contributes to repression of Major Histocompatibility Complex class II transcription

Project description:The multi-subunit CCR4 (carbon catabolite repressor 4)-NOT (Negative on TATA) complex serves as a central coordinator of all different steps of eukaryotic gene expression. Accordingly, members of the CCR4-NOT complex have been implicated in a variety of biological functions. Here we performed a systematic and comparative analysis of cells where the CCR4-NOT subunits CNOT1, CNOT2 or CNOT3 were individually downregulated using doxycycline-inducible shRNAs. Microarray experiments showed that downregulation of either CNOT subunit resulted in elevated expression of major histocompatibility complex class II (MHC II) target genes which are found in a gene cluster on chromosome 6. Increased expression of MHC II genes after knock-down or knock-out of CNOT subunits was seen in a variety of cell systems and also in naïve macrophages from CNOT3 conditional knock-out mice. CNOT2-mediated repression of MHC II genes occurred independent from the master regulator class II transactivator (CIITA) and detectable changes of the chromatin structure at the chromosomal MHC II locus. CNOT2 downregulation resulted in an increased de novo transcription of mRNAs and tethering of CNOT2 to a regulatory region governing MHC II expression resulted in dimished transcription. These results expand the known repertoire of CCR4-NOT members for immune regulation and identify CNOT proteins as a novel group of corepressors serving to restrict inappropriate or exaggerated class II expression, which can be causative for various diseases.

2017-03-15 | GSE90474 | GEO

Rate of recipient-derived alveolar macrophages development and major histocompatibility complex cross-dressing after lung transplantation in humans

Project description:Rate of recipient-derived alveolar macrophages development and major histocompatibility complex cross-dressing after lung transplantation in humans

| PRJNA728466 | ENA

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