Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA391483 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Shared αβ T Cell Receptor Usage in Lungs of Sarcoidosis Patients with Löfgren’s Syndrome [scPCR]
| PRJNA392200 | ENA
Project description:Shared αβ T Cell Receptor Usage in Lungs of Sarcoidosis Patients with Löfgren’s Syndrome [ePCR]
| PRJNA392107 | ENA
Project description:Shared αβ T Cell Receptor Usage in Lungs of Sarcoidosis Patients with Löfgren’s Syndrome
| PRJNA392108 | ENA
Project description:Sarcoidosis, a systemic granulomatous syndrome invariably affecting the lung, typically spontaneously remits but in ~20% of cases progresses with severe lung dysfunction or cardiac and neurologic involvement (complicated sarcoidosis). Unfortunately, current biomarkers fail to distinguish patients with remitting (uncomplicated) sarcoidosis from other fibrotic lung disorders, and fail to identify individuals at risk for complicated sarcoidosis. We utilized genome-wide peripheral blood gene expression analysis to identify a gene signature distinguishing sarcoidosis from healthy controls, which also served as a molecular signature for complicated sarcoidosis. Total RNA was isolated from PBMCs using standard molecular biology protocols without DNA contamination or RNA degradation. Sample processing (e.g., cDNA generation, fragmentation, end labeling, hybridization to Affymetrix GeneChip Human Exon 1.0 ST arrays) was performed per manufacturer’s instructions. A total of 29 African descent American (AA) and 10 European descent American (EA) patients with sarcoidosis were included in the overall sarcoidosis cohort with 18 AA and 4 EA patients diagnosed with complicated sarcoidosis.
2012-06-30 | E-GEOD-37912 | biostudies-arrayexpress
Project description:Sarcoidosis, a systemic granulomatous syndrome invariably affecting the lung, typically spontaneously remits but in ~20% of cases progresses with severe lung dysfunction or cardiac and neurologic involvement (complicated sarcoidosis). Unfortunately, current biomarkers fail to distinguish patients with remitting (uncomplicated) sarcoidosis from other fibrotic lung disorders, and fail to identify individuals at risk for complicated sarcoidosis. We utilized genome-wide peripheral blood gene expression analysis to identify a gene signature distinguishing sarcoidosis from healthy controls, which also served as a molecular signature for complicated sarcoidosis.
2012-07-01 | GSE37912 | GEO
Project description:Introduction: Sarcoidosis is a multisystem immuno-inflammatory disorder of unknown etiology that most commonly involves the lungs. We hypothesized that an unbiased approach to identify pathways activated in alveolar macrophagesâa key immuno-inflammatory cell in the lungâcan shed light on the pathogenesis of this complex disease. Methods: We recruited 15 patients with various stages of sarcoidosis and 12 healthy controls. All subjects underwent bronchoscopy with lavage. For each subject, total RNA was extracted from bronchoalveolar (BAL) cells and hybridized to an Affymetrix GeneChip Human Genome U133A 2.0 microarray. Rigorous statistical methods were applied to identify differential gene expression between subjects with sarcoidosis vs. controls. To better elucidate pathways differentially activated between these groups, we applied gene set enrichment analysis (GSEA) to the transcriptional profiles of BAL cells. We used false discovery rate (FDR) < 0.01 to designate significant enrichment. Results: Sarcoid patients were either non-smokers or ex-smokers, all had lung involvement and only 2 were on systemic prednisone. Healthy controls were all non-smokers. Comparison of BAL cell gene expression between sarcoidosis and healthy subjects revealed over 1200 differentially expressed genes at an FDR cutoff < 0.01. Several previously described immune mediators, such as interferon gamma, were up-regulated in the sarcoidosis subjects. Since genes often exert their influence through functionally coherent modules, we performed GSEA based on global expression profiles of alveolar macrophages between the subject groups. We identified more than 200 gene sets enriched in patients with sarcoidosis whereas very few pathways were over-represented in the healthy controls. Many of the sarcoidosis-associated pathways mapped to inflammatory and immune-related processes including T-cell signaling, graft vs. host disease, IL-12, IL-23, and IL-17 pathways, and oxidative phosphorylation. However, we also found and confirmed significant alteration in Proteasome-related pathways. Conclusions: BAL cells in sarcoidosis are characterized by enrichment of distinct transcriptional networks involved in immuno-inflammatory and proteasomal processes. Our findings add to the growing evidence implicating airspace resident cells in the pathogenesis of sarcoidoisis and identify specific pathways whose activation may modulate disease progression. Total RNA from BAL cells of 15 subjects with sarcoidosis and 12 healthy controls was hybridized to 27 Affymetrix Genechip Human U133A 2.0 microarrays
2016-07-22 | E-GEOD-75023 | biostudies-arrayexpress
Project description:Using 8-plex iTRAQ labelling exosmes isolated from bronchial lavage (BALF) were analyzed by LC-MS/MS. The measurements compared control subjects with sarcoidosis patients (15 in all) ; five with löfgrens syndrome and 10 with regular sacroidosis
2016-09-27 | PXD001808 | Pride
Project description:Expansions of CD4+ T cells utilizing TRAV12-1 and TRBV2 were found exclusively in HLA-DR3+ LS patients. These TCRs shared CDR3 homology, suggesting that these T cells are responsible for recognizing sarcoidosis-associated antigen(s) and are involved in the local alveolitis.
2017-07-21 | GSE100557 | GEO
Project description:Expansions of CD4+ T cells utilizing TRAV12-1/TRBV2 were found exclusively in HLA-DR3+ LS patients. These TCRs shared CDR3 homology, suggesting that these T cells are responsible for recognizing sarcoidosis-associated antigen(s) and are involved in the local alveolitis.
2017-07-21 | GSE100556 | GEO
Project description:Expansions of CD4+ T cells utilizing TRAV12-1 and TRBV2 were found exclusively in HLA-DR3+ LS patients. These TCRs shared CDR3 homology, suggesting that these T cells are responsible for recognizing sarcoidosis-associated antigen(s) and are involved in the local alveolitis.
2017-07-21 | GSE100378 | GEO