Homo sapiens
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ABSTRACT:
PROVIDER: PRJNA167199 | ENA |
REPOSITORIES: ENA
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Project description:HLA-B27-associated inflammatory diseases remains one of the strongest HLA-disease known to date. HLA-B27-associated acute anterior uveitis has wide-ranging medical significance due to its ocular, systemic, immunologic, and genetic features. To investigate the genes and signalling pathways located upstream of the inflammatory processes in HLA-B27-associated acute anterior uveitis will help to know the mechanism of this disease. HLA-B27-positive and -negative monocytes isolated from human peripheral blood were stimulated with Vibrio cholera lipopolysaccharide (LPS). Gene expression microarrays were used to identify the differentially expressed genes, and they were analysed by a series of bioinformatics-based techniques. Gene expression microarray analysis revealed marked differences between B27-positive monocytes in the genes that are upregulated in response to LPS stimulation. Gene Ontology enrichment (GO) and pathway analysis indicated that genes participating in protein transport and folding were essential to the inflammatory process. The LPS receptor, TLR4, induced the Toll-like receptor signalling pathway and pathways related to Vibrio cholerae infection, which are located upstream of the network and contribute to the overall response. Among the DE genes, PIK3CA, PIK3CB, AKT3, and MAPK1 may play critical roles in inflammation.Equivalent LPS stimulation induces a different response in HLA-B27-positive monocytes compared to monocytes lacking this HLA protein, suggesting that the TLR pathway is involved in the pathogenesis of HLA-B27-associated AAU. Blocking this pathway and other pathways by siRNA interference of candidate genes may contribute to the development of a treatment for this type of AAU. HLA-B27-positive monocytes isolated from human peripheral blood were stimulated with Vibrio cholera lipopolysaccharide (LPS) for 12 hours.
2012-05-31 | E-GEOD-37588 | biostudies-arrayexpress
Project description:HLA-B27-associated inflammatory diseases remains one of the strongest HLA-disease known to date. HLA-B27-associated acute anterior uveitis has wide-ranging medical significance due to its ocular, systemic, immunologic, and genetic features. To investigate the genes and signalling pathways located upstream of the inflammatory processes in HLA-B27-associated acute anterior uveitis will help to know the mechanism of this disease. HLA-B27-positive and -negative monocytes isolated from human peripheral blood were stimulated with Vibrio cholera lipopolysaccharide (LPS). Gene expression microarrays were used to identify the differentially expressed genes, and they were analysed by a series of bioinformatics-based techniques. Gene expression microarray analysis revealed marked differences between B27-positive monocytes in the genes that are upregulated in response to LPS stimulation. Gene Ontology enrichment (GO) and pathway analysis indicated that genes participating in protein transport and folding were essential to the inflammatory process. The LPS receptor, TLR4, induced the Toll-like receptor signalling pathway and pathways related to Vibrio cholerae infection, which are located upstream of the network and contribute to the overall response. Among the DE genes, PIK3CA, PIK3CB, AKT3, and MAPK1 may play critical roles in inflammation.Equivalent LPS stimulation induces a different response in HLA-B27-positive monocytes compared to monocytes lacking this HLA protein, suggesting that the TLR pathway is involved in the pathogenesis of HLA-B27-associated AAU. Blocking this pathway and other pathways by siRNA interference of candidate genes may contribute to the development of a treatment for this type of AAU.
2012-06-01 | GSE37588 | GEO
Project description:Uveitis describes a heterogeneous group of inflammatory eye diseases characterized by infiltration of leukocytes into the uveal tissues. uveitis associated with the HLA haplotype B27 (HLA-B27) is a common subtype of uveitis and a prototypical ocular immune-mediated disease. Local immune mechanisms driving human uveitis are poorly characterized mainly due to the limited available biomaterial and subsequent technical limitations. Here, we provide the first high-resolution characterization of intraocular leukocytes in HLA-B27 positive (n=3) and negative (n=2) anterior uveitis and an infectious endophthalmitis control (n=1) by combining single cell RNA-sequencing with flow cytometry and protein analysis. Ocular cell infiltrates consisted primarily of lymphocytes in both subtypes of uveitis and of myeloid cells in infectious endophthalmitis. HLA-B27 positive uveitis exclusively featured a plasmacytoid and classical dendritic cells (cDC) infiltrate. Moreover, cDCs were central in predicted local cell-cell communication. This suggests a unique pattern of ocular leukocyte infiltration in HLA-B27 positive uveitis with relevance of dendritic cells.
2021-06-25 | GSE178833 | GEO
Project description:Intra-ocular dendritic cells characterize HLA-B27-associated acute anterior uveitis
| PRJNA741216 | ENA
Project description:Associations of the Intestinal Microbiome and HLA-B27-associated anterior uveitis
| PRJEB55787 | ENA
Project description:RNA-sequencing data from flow cytometry-sorted primary HLA-DR+ Lin-(CD19-CD3-CD14-) CD1c+ cDC2s purifed from frozen peripheral blood mononuclear cells from patients with anterior, intermediate, and posterior non-infectious uveitis and healthy controls.
2022-01-29 | GSE195501 | GEO
Project description:Pathogenesis of anterior uveitis (ocular manifestation of ZIKV infection in adults, distinct from children).
2021-03-03 | GSE131605 | GEO
Project description:HLA-B27 is a class I major histocompatibility (MHC-I) allele that confers susceptibility to the rheumatic disease ankylosing spondylitis (AS) by an unknown mechanism. ERAP1 is an aminopeptidase that trims peptides in the endoplasmic reticulum for binding to MHC-I molecules. ERAP1 shows genetic epistasis with HLA-B27 in conferring susceptibility to AS. Male HLA-B27 transgenic rats develop arthritis and serve as an animal model of AS, whereas female B27 transgenic rats remain healthy. We used large-scale quantitative mass-spectrometry to identify over 15,000 unique HLA-B27 peptide ligands, isolated after immunoaffinity purification of the B27 molecules from the spleens of HLA-B27 transgenic rats. Heterozygous deletion of ERAP1, which reduced ERAP1 level to less than half, had no qualitative or quantitative effects on the B27 peptidome. Homozygous deletion of ERAP1 affected approximately one third of the B27 peptidome, but left most of the B27 peptidome unchanged, suggesting the possibility that some of the HLA-B27 immunopeptidome is not processed in the presence of ERAP1. Deletion on ERAP1 was permissive for the AS-like phenotype. Deletion of ERAP1 increased mean peptide length, and increased the frequency of C-terminal hydrophobic residues and of N-terminal Ala, Ser or Lys. The presence of ERAP1 increased the frequency of C-terminal Lys and Arg, of Glu and Asp at intermediate residues, and of N-terminal Gly. Several peptides of potential interest in AS pathogenesis, previously identified in human cell lines, were isolated. However, rats susceptible to arthritis had B27 peptidomes similar to those of non-susceptible rats, and no peptides were found to be uniquely associated with arthritis. Whether specific B27-bound peptides are required for AS pathogenesis remains to be determined.
2017-02-13 | PXD005502 | Pride
Project description:In HLA-B27/human beta-2m transgenic rat (B27-rats), the spontaneous development of a chronic inflammatory disorder closely resembling spondyloarthritis (SpA) is strongly correlated with high levels of HLA-B27/human beta-2m transgene expression and with aberrant function of dendritic cells (DCs). To dissect the mechanisms that could be involved in DCs dysfunction, we investigated the genes expression by transcriptomic analysis in DCs from B27 versus controls rats
2014-01-17 | E-MEXP-3808 | biostudies-arrayexpress
Project description:Enthesitis-related arthritis (ERA) is a subtype of juvenile idiopathic arthritis (JIA) with enthesitis and sacroiliitis, which differ from other types of JIA in symptoms, pathogenesis, and outcome. Although the association of human leukocyte antigen-B27 (HLA-B27) with ERA has been confirmed for decades, the pathogenesis of ERA is poorly understood. Here, we performed single-cell RNA-seq of 1,73,134 mononuclear cells extricated from patients with oligoarthritis (OligoA) or ERA and integrated 58,725 PBMCs of healthy people to profile the immune characteristic that discriminates ERA from OligoA. We found that conventional type 1 dendritic cells (cDC1s) were enriched in the joints of patients with ERA and exhibited a high level of MHC class I antigen presentation. Central memory CD8+ T cells critically contributed to the elevation of XCL1, recruiting XCR1+ cDC1 in joints of ERA. Flow cytometry and enzyme-linked immunosorbent assay (ELISA) analyses confirmed an increased proportion and interaction of cDC1s and CD8+ T cells. In addition, macrophages occupied the causal position in the pathogenesis of OligoA, along with high expression of MHC class II molecules on macrophages and cDC2s in the joints. This study suggests that the positive feedback between cDC1s and CD8+ T cells is a key mediator of HLA-B27-positive arthritis pathogenesis.
2026-02-22 | GSE213095 | GEO