Project description:Macrophages, which populate barrier tissues already in the embryo, are primary targets for CMV. Upon infection macrophages undergo a morphological, immunophenotypic and metabolic transformation process with features of stemness, altered migration, enhanced invasiveness and provision of the cell cycle machinery to viral proliferation.
Project description:Macrophages, which populate barrier tissues already in the embryo, are primary targets for CMV. Upon infection macrophages undergo a morphological, immunophenotypic and metabolic transformation process with features of stemness, altered migration, enhanced invasiveness and provision of the cell cycle machinery to viral proliferation.
Project description:Macrophages, which populate barrier tissues already in the embryo, are primary targets for CMV. Upon infection macrophages undergo a morphological, immunophenotypic and metabolic transformation process with features of stemness, altered migration, enhanced invasiveness and provision of the cell cycle machinery to viral proliferation.
Project description:The objective of this study was to characterise macrophage subsets in bone marrow (BM) isolated from Csf1r-EGFP mice. A concurrent imaging flow cytometry study conducted by our team unexpectedly revealed macrophage surface marker staining emanates from membrane-bound subcellular remnants associated with unrelated cells. Expression data from sorted BM “macrophage” populations was found to be consistent with macrophage fragments associated with non-macrophage cells. Granulocyte-specific genes were enriched within the CD11b+ “macrophage” (CD11b+F4/80+Ly6G-GFPloVCAM1+) populations, whereas CD11b- “macrophages” (CD11b-F4/80+GFP+VCAM1+) were consistent with a mixed cell population including both plasma cells and erythroblasts. This data demonstrates how fragmentation of hematopoietic tissue macrophages can result in misattribution of macrophage identity to non-macrophage populations, thereby undermining accuracy of macrophage ex vivo molecular profiles.
Project description:Tissue-resident macrophages comprise heterogeneous populations with unique functions and distinct gene expression signatures. While it has been established that they mostly originate from embryonic progenitors, the signals inducing a characteristic tissue-specific differentiation program remain unknown. Here we identify PPARγ as the crucial transcription factor determining perinatal alveolar macrophage (AM) development and identity. Development of the fetal monocyte derived AM precursor was largely abrogated in CD11c-Cre/Ppargfl/fl mice. To reveal the underlying changes in gene expression, we performed microarray analysis of sorted WT and KO AM and pre-AM from 3 different timepoints. Part2: adult sorts & array AM FACS-sorted from lungs of adult PPARgfl/fl (WT) and CD11c-cre/PPARgfl/fl (KO) mice and subsequently processed for RNA extraction and hybridization on Affymetrix microarrays. 2 biological replicates per group, each composed of pooled cells from 2 individual mice