MiRNA in CD4+ T cells: control vs. patients with myasthenia gravis
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ABSTRACT:
PROVIDER: PRJNA438450 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:To investigate the abnormal expression amount of microRNAs in T cells of patients with myasthenia gravis
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Project description:Identification of deregulated genes in the thymus of myasthenia gravis patients' subgroup.
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Project description:Autoimmune myasthenia gravis (MG) is characterized by thymic abnormalities such as hyperplasia and thymoma. Thymus plays an important role in self-tolerance and is involved in initiation and progression of the disease. A large proportion of MG patient show the presence of ectopic germinal centers (GC) in thymus that are absent in normal individuals. However, the exact mechanism how this change in thymus morphology is triggered and if this is related to pathophysiology of the disease remains unknown. In this study we have compared the mRNA profile of thymus samples obtained during a clinical trial (Thymectomy Trial in Non-Thymomatous Myasthenia Gravis Patients Receiving Prednisone Therapy. ClinicalTrials.gov Identifier: NCT00294658). We have compared the miRNA profile of thymus samples that have distinct germinal centers with those that lack them using Affymetrix miRNA array 4.0 to identify the differentially expressed genes with in the two groups.
2017-09-14 | GSE103812 | GEO
Project description:Myasthenia gravis (MG) is an autoimmune disease affecting the neuromuscular junction, whose clinical hallmark is muscle weakness and early fatigability. Azathioprine (AZA) is commonly used in Myasthenia Gravis therapy. AZA is a purine antagonist, which inhibits the cell cycle in the resting and DNA synthesis phases. It is usually used as an immunosuppressant to block T- and B-cell proliferation. AZA, bioconverted to 6-mercaptopurine by glutathione S-transferase (GST), can be metabolized either through the hypoxanthine phosphoribosyl transferase pathway to active 6-thioguanine nucleotides (6-TGN) or through the thiopurine S-methyltransferase (TPMT) pathway to inactive methyl-thiopurine metabolites. The incorporation of active 6-TGNs into DNA, causing breaks in DNA strands resulting in interference with RNA production and thereby protein synthesis, is responsible for the drug effect. The response to AZA is determined by which metabolic pathway is being favored. While balanced use of both HPRT and TPMT pathways results in responsiveness to AZA, hyperactivity of TPMT skews the balance towards the TPMT pathway and results in unresponsiveness to AZA with no pharmacological effect. In contrast, low TPMT activity skews the balance towards the HPRT pathway, resulting in increasing side-effects due to the accumulation of 6-TGNs. Current treatments for MG therapy are often inadequate because less than 40% of patients achieve complete remission with available drugs. This reflects the lack of drugs acting on target sites for which there is strong evidence of pathogenicity and the inability to identify responder patients. No criteria for responsiveness are available, exposing patients to unpredictable failures and unpredictable side effects. These individuals are at particular risk for adverse drug reaction (ADRs) or therapeutic failure. Genetic profiling with the Affymetrix drug metabolizing enzymes and transports genotyping array offers the ability to determine 1,931 variants and 225 genes involved in drug metabolism and disposition. Accordingly, the study of well-known drug-metabolizing genes can be involved in the specific metabolic pathway of a drug, which is more likely to define genotype-phenotype association and thereby genotype profiles relevant to drug response that can be applied as predictive biomarkers for pharmacological treatment.
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Project description:Autoimmune myasthenia gravis (MG) is characterized by thymic abnormalities such as hyperplasia and thymoma. Thymus plays an important role in self-tolerance and is involved in initiation and progression of the disease. A large proportion of MG patient show the presence of ectopic germinal centers (GC) in thymus that are absent in normal individuals. However, the exact mechanism how this change in thymus morphology is triggered and if this is related to pathophysiology of the disease remains unknown. In this study we have compared the mRNA profile of thymus samples obtained during a clinical trial (Thymectomy Trial in Non-Thymomatous Myasthenia Gravis Patients Receiving Prednisone Therapy. ClinicalTrials.gov Identifier: NCT00294658). We have compared the mRNA profile of thymus samples that have distinct germinal centers with those that lack them using Affymetrix human transcriptome array 2.0 to identify the differentially expressed genes with in the two groups.
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Project description:The project was focused on the serum proteomic profiling of the neuromuscular autoimmune disease, Myasthenia gravis (MG). The project aimed to identify candidate serum proteins to understand the disease better. To eliminate any typical autoimmune response Rheumatoid arthritis (RA) was included as a reference disease to the sample group.
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Project description:gene expression profile in diaphragm (DIA), extensor digitorum longus (EDL) and extraocular (EOM) muscles of rats with actively induced experimentally acquired MG (EAMG) using Affymetrix rat RAE230 gene chip. Keywords: myasthenia gravis (MG), rats with actively induced experimentally acquired MG (EAMG)
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Project description:Myasthenia gravis (MG) is a chronic antibody-mediated autoimmune disease disrupting neuromuscular synaptic transmission. Antibodies (Abs) against the acetylcholine receptor (AChR) are detected in approximately 85% of patients. Here, we aimed to study the serum proteome of MG and to identify novel biomarkers reflecting disease activity.
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Project description:Gene expression profiling of thymus samples from myasthenia gravis patients.
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