Similar Datasets
Project description:To assess the impact of Drosha on the response to IFNB
2017-06-28 | GSE96889 | GEO
Project description:Astrocyte-microglia crosstalk via CSF1 and IFNb promotes central nervous system repair
| PRJNA1447364 | ENA
Project description:Curcumin is a potent modulator of the inflammatory transcriptome in microglia We have performed global gene expression analysis of BV-2 microglial cells under the following conditions: untreated, 20 µM Curcumin-treated, 100ng/ml LPS-treated, or 20 µM Curcumin-treated + 100ng/ml LPS-treated
2010-09-29 | E-GEOD-23639 | biostudies-arrayexpress
Project description:This experiment set is used for the manuscript entitled: Pharmacogenomics of Interferon-b therapy in multiple sclerosis: Baseline IFN signature determines pharmacological differences between patients. In this study we generated and analyzed pre- and post- IFNb treatment gene expression patterns of RRMS patients with the aim of identifying pre-existing and/or drug-induced signatures that will allow us to make predictions on the expected pharmacological effects of IFNb treatment. We show that the expression level of IFN response genes prior to treatment, determines the pharmacological differences between patients with MS at the molecular level. A group of 16 Dutch patients (10 females and 6 males) with clinically definite relapsing-remitting MS was recruited from the outpatient clinic of the MS Centre Amsterdam. Mean age at start of IFNb therapy is 40.6 +/- 7.7, mean EDSS is 2.3 +/- 1.3 (range 1-6). Blood samples were obtained just before treatment and 1 month after start of the therapy. Patients received Avonex, Betaferon, Rebif 22 or Rebif 44. A compound treatment design type is where the response to administration of a compound or chemical (including biological compounds such as hormones) is assayed. Compound Based Treatment: Before and 1 month after IFNb therapy Keywords: compound_treatment_design Complex
2008-04-01 | E-GEOD-10655 | biostudies-arrayexpress
Project description:This experiment set is used for the manuscript entitled: Pharmacogenomics of Interferon-b therapy in multiple sclerosis: Baseline IFN signature determines pharmacological differences between patients. In this study we generated and analyzed pre- and post- IFNb treatment gene expression patterns of RRMS patients with the aim of identifying pre-existing and/or drug-induced signatures that will allow us to make predictions on the expected pharmacological effects of IFNb treatment. We show that the expression level of IFN response genes prior to treatment, determines the pharmacological differences between patients with MS at the molecular level. A group of 16 Dutch patients (10 females and 6 males) with clinically definite relapsing-remitting MS was recruited from the outpatient clinic of the MS Centre Amsterdam. Mean age at start of IFNb therapy is 40.6 +/- 7.7, mean EDSS is 2.3 +/- 1.3 (range 1-6). Blood samples were obtained just before treatment and 1 month after start of the therapy. Patients received Avonex, Betaferon, Rebif 22 or Rebif 44. A compound treatment design type is where the response to administration of a compound or chemical (including biological compounds such as hormones) is assayed. Compound Based Treatment: Before and 1 month after IFNb therapy Keywords: compound_treatment_design
2008-04-01 | GSE10655 | GEO
Project description:In the brain the cells that control inflammation are called a type of white blood cell called microglia. Microglia are located throughout the brain and spinal cord and account for 10–15% of all cells found within the brain. As the resident white blood cells, they are the main active immune defence in the central nervous system (CNS). Microglia are part of an important class of cells known as macrophages that have two main states: M1 and M2. M1 cells are pro- inflammatory, leading to more inflammation, while M2 are anti-inflammatory, and drive wound healing. In this study, we will collect primary microglia from surgical biospies of 100 individuals.
This data is part of a pre-publication release. For information on the proper use of pre-publication data shared by the Wellcome Trust Sanger Institute (including details of any publication moratoria), please see http://www.sanger.ac.uk/datasharing/
| EGAS00001002494 | EGA
Project description:Iron accumulation in microglia has been observed in Alzheimer’s disease and other neurodegenerative disorders and is thought to contribute to disease progression through various mechanisms including neuroinflammation. To study the interaction between iron accumulation and inflammation, we treated human induced pluripotent stem cell-derived microglia (iPSC-MG) with an increasing concentration of iron, in combination with inflammatory stimuli such as interferon gamma and amyloid β, and performed RNA sequencing.
| EGAS00001006112 | EGA
Project description:To determine the impact of MEM40 and IFNB on normal human donor monocyte-derived DCs (Mo-DCs) phenotype, we used an experimental design where human A549 lung cancer cells were first infected with Ad-Null or adenoviruses expressing human IFNB, MEM40 or MEM40 + IFNB, followed by removal of virus-containing supernatant and co-culture with Mo-DCs. We used the above design followed by sorting of MHC-II+ CD11c+ cells for bulk RNA-sequencing.
2023-02-13 | GSE223342 | GEO
Project description:Interferon-b (IFN-b) belongs to the type I interferon family of cytokines and via binding to its receptor, interferon-a/b-receptor (IFNAR), it exerts immunoregulatory effects such as anti-viral and anti-inflammatory properties, and clinical benefits for patients with the CNS disease multiple sclerosis. To compare differentially regulated genes in neurons of interferon-beta knock out mice (Ifnb–/–), we conducted a microarray analysis on cerebellar granular neurons (CGNs) from wt (Ifnb+/+) and Ifnb-/- mice with or without treatment with recombinant IFN-b.
2015-10-08 | GSE63815 | GEO
Project description:Curcumin is a potent modulator of the inflammatory transcriptome in microglia
2010-09-29 | GSE23639 | GEO