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The lupus susceptibility allele DRB1*03:01 encodes a disease driving epitope [THP-1]

ABSTRACT: The lupus susceptibility allele DRB1*03:01 encodes a disease driving epitope [THP-1]

PROVIDER: PRJNA727352 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14423952.fastq.gz	Fastqsanger.gz
	SRR14423953.fastq.gz	Fastqsanger.gz
	SRR14423954.fastq.gz	Fastqsanger.gz
	SRR14423955.fastq.gz	Fastqsanger.gz
	SRR14423956.fastq.gz	Fastqsanger.gz

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The lupus susceptibility allele DRB1*03:01 encodes a disease driving epitope [THP-1]

Project description:We report RNA sequencing data that shows the differential effects of HLA-DRb1*0301 (LE), HLA-DRb1*0401 (SE) and HLA-DRb1*0402 (PE) on macrophage gene expression under IFNγ cell culture conditions.

2022-08-03 | GSE173876 | GEO

The lupus susceptibility allele DRB1*03:01 encodes a disease driving epitope [RAW264.7]

2022-08-03 | GSE173875 | GEO

The lupus susceptibility allele DRB1*03:01 encodes a disease driving epitope

Project description:The lupus susceptibility allele DRB1*03:01 encodes a disease driving epitope

| PRJNA727339 | ENA

The lupus susceptibility allele DRB1*03:01 encodes a disease driving epitope [RAW264.7]

Project description:The lupus susceptibility allele DRB1*03:01 encodes a disease driving epitope [RAW264.7]

| PRJNA727351 | ENA

The lupus susceptibility allele DRB1*03:01 encodes a disease-driving epitope.

Project description:The HLA-DRB1*03:01 allele is a major genetic risk factor in systemic lupus erythematosus (SLE), but the mechanistic basis of the association is unclear. Here we show that in the presence of interferon gamma (IFN-γ), a short DRB1*03:01-encoded allelic epitope activates a characteristic lupus transcriptome in mouse and human macrophages. It also triggers a cascade of SLE-associated cellular aberrations, including endoplasmic reticulum stress, unfolded protein response, mitochondrial dysfunction, necroptotic cell death, and production of pro-inflammatory cytokines. Parenteral administration of IFN-γ to naïve DRB1*03:01 transgenic mice causes increased serum levels of anti-double stranded DNA antibodies, glomerular immune complex deposition and histopathological renal changes that resemble human lupus nephritis. This study provides evidence for a noncanonical, antigen presentation-independent mechanism of HLA-disease association in SLE and could lay new foundations for our understanding of key molecular mechanisms that trigger and propagate this devastating autoimmune disease.

| S-EPMC9334592 | biostudies-literature

The lupus susceptibility allele DRB1*03:01 encodes a disease driving epitope

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-08-03 | GSE173877 | GEO

New Allele HLA-DRB1*03

Project description:Sample od DVMO Brasil, with new allele HLA-DRB1*03.

| PRJEB41331 | ENA

The HLA-DRB1*03:01 ligandome is highly conserved on N- and C-terminal residues outside the peptide-binding cleft

Project description:Human CD4+ T lymphocytes play an important role in inducing potent immune responses. They are activated and stimulated by peptides presented in Major Histocompatibility Complex Class II molecules. These MHC class II molecules typically present peptides of between 12 and 20 amino acids in length. The region that interacts with the MHC molecule, designated as the binding core, is highly conserved in the residues which anchor the peptide to the molecule. In addition, as these peptides are the product of proteolytic cleavages, certain conserved residues may be expected at the N- and C-termini outside the binding core. To study whether similar conserved residues are present in different types of cells , the ligandomes of HLA-DRB1*03:01 derived from two different cell types (dendritic cells and EBV-transformed B-cells) were identified with mass spectrometry and the binding core and N- and C-terminal residues were analysed using the frequencies of the amino acids in the human proteome. Similar binding motifs were found as well as comparable conservations in the N- and C-terminal residues. Furthermore, these terminal conservations of the HLA-DRB1*03:01 ligandome were compared to the N- and C-terminal conservations of the HLA-DRB1*04:01 ligandome acquired from dendritic cells. Again, comparable conservations were evident with only minor differences. Taken all together, these analyses show that there are conservations in the terminal residues of peptides, presumably the result of the activity of proteases involved in antigen processing.

2019-09-16 | PXD014253 | Pride

New Allele HLA-DRB1

Project description:HLA-DRB1*11:04 new

| PRJEB64134 | ENA

Overexpression of hsa-HLA-DRB1 may play a role in diabetic foot ulcers by regulating miRNA_12118 and FLT-1

Project description:Introduction: We investigated the role and mechanism of hsa-HLA-DRB1 in the development and progression of diabetic foot ulcers. Methods: High-throughput sequencing was performed on three normal foot trauma tissues and diabetic foot ulcer tissues. The circRNAs with significant differences were identified. The downstream miRNAs were predicted by miRanda and RNAhybrid databases, and the mRNAs were predicted by the TargetScan database. Validation was performed with CCK8, flow cytometry, trabecular scratch assay, tubule generation assay, Western blot, dual luciferase assay, and RT-qPCR. Results: High-throughput sequencing identified 461 significantly different circRNAs, of which 260 were up-regulated and 201 down-regulated. Compared to normal tissue, hsa-HLA-DRB1 was highly expressed in diabetic foot ulcers. The hsa-HLA-DRB1/miRNA_12118/FLT-1 axis was constructed. In vitro, we found that HLA-DRB1 overexpression inhibited cell viability, wound healing, and tubule formation, promoted apoptosis, and enhanced FLT-1 expression in HUVECs. Conclusion: The upregulation of hsa-HLA-DRB1 may promote diabetic foot development by targeting miRNA_12118 and acting on FLT-1. Therefore, our study highlights the key role of the hsa-HLA-DRB1/miRNA_12118/FLT-1 axis in diabetic foot trauma.

2025-06-04 | GSE286165 | GEO

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