Project description:Comparison of the transcriptome macrophages derived from CD14+ human monocyte-derived macrophages generated in the presence of M-CSF (M-Mphage) or GM-CSF (GM-Mphage) and MTX.
Project description:Macrophage phenotypic and functional heterogeneity derives from tissue-specific transcriptional signatures shaped by the local microenvironment. M-CSF drives the generation of human monocyte-derived macrophages with a potent anti-inflammatory activity upon stimulation. One-carbon metabolism (OCM) is a complex network of biosynthetic pathways that includes de novo biosynthesis of purines and thymidylate, amino acid metabolism, and methylation reactions. We explored the molecular impact of blocking OCM with high-doses of the anti-folate methotrexate (MTX) on the gene expression profile in M-CSF-primed human monocyte derived macrophages.
Project description:DC, monocyte and macrophage networks are evolutionarily conserved but the distinct subsets have been difficult to distinguish due to shared overlapping phenotypic markers between the cells. Using transcriptome microarray profiling of human and mouse mononuclear phagocyte subsets, we have distinguished human dermal DCs from monocyte-derived cells and macrophages. Gene Expression from total RNA from human dermal macrophages, epidermal LCs and CD14+ cells subsets purified by FACS
Project description:Identification of genes differentially expressed between human monocyte-macrophages generated in the presence of either GM-CSF (termed M1) or M-CSF (termed M2) and in the presence (+MTX) or absence (-) of Methotrexate
Project description:Identification of genes differentially expressed between human monocyte-macrophages generated in the presence of either GM-CSF (termed M1) or M-CSF (termed M2) and in the presence (+MTX) or absence (-) of methotrexate
Project description:To study effects of IFNalpha treatment on monocyte-derived macrophages which may influence susceptibility or resistance to HIV. Experiment Overall Design: Human monocyte-derived macrophages were stimulated with IFNalpha and analyzed for global gene expression.