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10X Genomics 10x genomics single cell transcriptomics
Data sources for advancing computational modeling “Not So Big” and “Big” data sources can be utilized collectively to build computational models of varying complexity. “Not So Big” data are usually disparate, require extensive data collation, and must be obtained individually from various literature sources in the form of data tables present in the supplementary material. The “Not So Big” data are derived from targeted and focused experiments and provides tissue-level detail for mechanistic models such as the first cell cycle gene regulatory network from Tyson (1991). Bulk and single-cell “Big” data are derived from targeted and unbiased assays, and are usually stored in annotated collections and compendiums such as GEO <t>(transcriptomics),</t> ArrayExpress (transcriptomics), MetaboLights (metabolomics), and PRIDE (proteomics). This “Big” data provides genome-scale detail for informing correlation networks and genome scale metabolic models. Single-cell “Big” data from reference atlases, including The Cancer Genome Atlas, the Human Cell Atlas, HuBMAP, and Tabula Sapiens , provide untargeted and unbiased assays at the whole-body physiological scale. These data can be utilized to inform future virtual human models at various scales, including the molecular level (i.e., Wnt/B-Catenin signaling pathway), single-cell level (i.e., gene correlation networks), and physiological level (i.e., multi-organ interactions). <xref ref-type=Figure 1 adapted from Tyson (1991), Gustafsson et al. (2023), Park et al. (2016), Moss et al. (2021). Created using biorender.com . " width="250" height="auto" />
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Article Title: From sampling to simulating: Single-cell multiomics in systems pathophysiological modeling

Journal: iScience

doi: 10.1016/j.isci.2024.111322

Data sources for advancing computational modeling “Not So Big” and “Big” data sources can be utilized collectively to build computational models of varying complexity. “Not So Big” data are usually disparate, require extensive data collation, and must be obtained individually from various literature sources in the form of data tables present in the supplementary material. The “Not So Big” data are derived from targeted and focused experiments and provides tissue-level detail for mechanistic models such as the first cell cycle gene regulatory network from Tyson (1991). Bulk and single-cell “Big” data are derived from targeted and unbiased assays, and are usually stored in annotated collections and compendiums such as GEO (transcriptomics), ArrayExpress (transcriptomics), MetaboLights (metabolomics), and PRIDE (proteomics). This “Big” data provides genome-scale detail for informing correlation networks and genome scale metabolic models. Single-cell “Big” data from reference atlases, including The Cancer Genome Atlas, the Human Cell Atlas, HuBMAP, and Tabula Sapiens , provide untargeted and unbiased assays at the whole-body physiological scale. These data can be utilized to inform future virtual human models at various scales, including the molecular level (i.e., Wnt/B-Catenin signaling pathway), single-cell level (i.e., gene correlation networks), and physiological level (i.e., multi-organ interactions). <xref ref-type=Figure 1 adapted from Tyson (1991), Gustafsson et al. (2023), Park et al. (2016), Moss et al. (2021). Created using biorender.com . " title="... in annotated collections and compendiums such as GEO (transcriptomics), ArrayExpress (transcriptomics), MetaboLights (metabolomics), and PRIDE (proteomics). This ..." property="contentUrl" width="100%" height="100%"/>
Figure Legend Snippet: Data sources for advancing computational modeling “Not So Big” and “Big” data sources can be utilized collectively to build computational models of varying complexity. “Not So Big” data are usually disparate, require extensive data collation, and must be obtained individually from various literature sources in the form of data tables present in the supplementary material. The “Not So Big” data are derived from targeted and focused experiments and provides tissue-level detail for mechanistic models such as the first cell cycle gene regulatory network from Tyson (1991). Bulk and single-cell “Big” data are derived from targeted and unbiased assays, and are usually stored in annotated collections and compendiums such as GEO (transcriptomics), ArrayExpress (transcriptomics), MetaboLights (metabolomics), and PRIDE (proteomics). This “Big” data provides genome-scale detail for informing correlation networks and genome scale metabolic models. Single-cell “Big” data from reference atlases, including The Cancer Genome Atlas, the Human Cell Atlas, HuBMAP, and Tabula Sapiens , provide untargeted and unbiased assays at the whole-body physiological scale. These data can be utilized to inform future virtual human models at various scales, including the molecular level (i.e., Wnt/B-Catenin signaling pathway), single-cell level (i.e., gene correlation networks), and physiological level (i.e., multi-organ interactions). Figure 1 adapted from Tyson (1991), Gustafsson et al. (2023), Park et al. (2016), Moss et al. (2021). Created using biorender.com .

Techniques Used: Derivative Assay

Molecularly targeted methods for single-cell and spatial  transcriptomics
Figure Legend Snippet: Molecularly targeted methods for single-cell and spatial transcriptomics

Techniques Used:

Examples of transcriptome-proteome multiomics technologies
Figure Legend Snippet: Examples of transcriptome-proteome multiomics technologies

Techniques Used: Single-cell Isolation, RNA Detection, Reverse Transcription, Mass Cytometry, Staining

Computational models informed by experimental data The components, interactions, correlations, and patterns extracted from “Big” data (multi-omics data including transcriptomics, proteomics, metabolomics, and spatial omics) and the components, interactions and mechanisms extracted from “Not So Big” data (i.e., western blots, immuno-staining, and qPCR) can be utilized to generate and inform molecular signaling networks, putative cellular networks, and gene regulatory networks. For instance, while the MAP kinase pathway was discovered using “Not So Big” data sources (solid line) many “Big” data sources (dashed line) have confirmed and further explained and complemented these initial findings. Similarly, while gene regulatory networks have been mainly developed using “Big” data (solid line), “Not So Big” data (dashed line) can also be informative when generating such networks. For example, Park et al., (2016) modeled neurons during the circadian cycle. First, five neuronal groups were identified according to their unique transcriptional landscapes with marker genes shown for each of the groups. A gene regulatory network was then developed based on the major molecular interactions between key neuropeptides (VIP, AVP, PROK2, and PACAP) and the neuronal groups. “Big” and “Not So Big” data (solid lines) have be analyzed in combination to identify putative cellular networks. Cell types can be identified within the “Big” data by using information from “Not So Big” data. Then, cell states within each cell type community can be determined by molecular markers. The cell types and states can then be used to infer cell state transitions, trajectories, and interactions. A greater influence of “Big” and “Not So Big” data on developing the various networks is shown with solid lines with lesser influence shown by dashed lines. GF: growth factor, GFR: growth factor receptor, VIP: Vasoactive Intestinal Peptide, AVP: Arginine Vasopressin, PROK2: Prokineticin 2, PACAP: Pituitary Adenylate Cyclase-Activating Polypeptide. Fig. adapted from Park et al., (2016). Created using biorender.com .
Figure Legend Snippet: Computational models informed by experimental data The components, interactions, correlations, and patterns extracted from “Big” data (multi-omics data including transcriptomics, proteomics, metabolomics, and spatial omics) and the components, interactions and mechanisms extracted from “Not So Big” data (i.e., western blots, immuno-staining, and qPCR) can be utilized to generate and inform molecular signaling networks, putative cellular networks, and gene regulatory networks. For instance, while the MAP kinase pathway was discovered using “Not So Big” data sources (solid line) many “Big” data sources (dashed line) have confirmed and further explained and complemented these initial findings. Similarly, while gene regulatory networks have been mainly developed using “Big” data (solid line), “Not So Big” data (dashed line) can also be informative when generating such networks. For example, Park et al., (2016) modeled neurons during the circadian cycle. First, five neuronal groups were identified according to their unique transcriptional landscapes with marker genes shown for each of the groups. A gene regulatory network was then developed based on the major molecular interactions between key neuropeptides (VIP, AVP, PROK2, and PACAP) and the neuronal groups. “Big” and “Not So Big” data (solid lines) have be analyzed in combination to identify putative cellular networks. Cell types can be identified within the “Big” data by using information from “Not So Big” data. Then, cell states within each cell type community can be determined by molecular markers. The cell types and states can then be used to infer cell state transitions, trajectories, and interactions. A greater influence of “Big” and “Not So Big” data on developing the various networks is shown with solid lines with lesser influence shown by dashed lines. GF: growth factor, GFR: growth factor receptor, VIP: Vasoactive Intestinal Peptide, AVP: Arginine Vasopressin, PROK2: Prokineticin 2, PACAP: Pituitary Adenylate Cyclase-Activating Polypeptide. Fig. adapted from Park et al., (2016). Created using biorender.com .

Techniques Used: Biomarker Discovery, Western Blot, Immunostaining, Marker

Computational models informed by single-cell omics (A) Single-cell omics, including transcriptomics, proteomics, and metabolomics can be used for modeling tumor cell differentiation dynamics. The specific cell types of interest that were identified within the tumor tissue include stem, progenitor, and differentiated cell types. State transitions, trajectories, and interactions between these cell types can then be inferred such that a network model can be generated. The tumor cell differentiation model can then be simulated to determine how the individual cell populations within the tumor change over time. (B) Single-cell omics experiments can be performed on the liver following resection to elucidate liver-specific cell types including Kupffer cells, Stellate cells and hepatocytes. For simplicity, we only show the hepatocyte cell states (replicating, quiescent, and primed), which are informed by molecular markers from the single-cell data. State transitions, trajectories and interactions can then be inferred from the cell states. A systems network model of liver regeneration can then be developed using the features extracted from the single-cell data and the model can be simulated for liver mass recovery and cellular dynamics. The total mass recovery as well as the populations of primed and replicating hepatocytes populations during regeneration are shown. Additionally, the populations of pro- and anti-regenerative stellate cell populations during regeneration are shown. <xref ref-type=Figure 4 A adapted from Nazari et al., (2018). Figure 4 B adapted from Cook et al., (2018). Created using biorender.com . " title="... informed by single-cell omics (A) Single-cell omics, including transcriptomics, proteomics, and metabolomics can be used for modeling ..." property="contentUrl" width="100%" height="100%"/>
Figure Legend Snippet: Computational models informed by single-cell omics (A) Single-cell omics, including transcriptomics, proteomics, and metabolomics can be used for modeling tumor cell differentiation dynamics. The specific cell types of interest that were identified within the tumor tissue include stem, progenitor, and differentiated cell types. State transitions, trajectories, and interactions between these cell types can then be inferred such that a network model can be generated. The tumor cell differentiation model can then be simulated to determine how the individual cell populations within the tumor change over time. (B) Single-cell omics experiments can be performed on the liver following resection to elucidate liver-specific cell types including Kupffer cells, Stellate cells and hepatocytes. For simplicity, we only show the hepatocyte cell states (replicating, quiescent, and primed), which are informed by molecular markers from the single-cell data. State transitions, trajectories and interactions can then be inferred from the cell states. A systems network model of liver regeneration can then be developed using the features extracted from the single-cell data and the model can be simulated for liver mass recovery and cellular dynamics. The total mass recovery as well as the populations of primed and replicating hepatocytes populations during regeneration are shown. Additionally, the populations of pro- and anti-regenerative stellate cell populations during regeneration are shown. Figure 4 A adapted from Nazari et al., (2018). Figure 4 B adapted from Cook et al., (2018). Created using biorender.com .

Techniques Used: Cell Differentiation, Generated

Highlighted algorithms for computational modeling informed by single-cell and spatial omics data
Figure Legend Snippet: Highlighted algorithms for computational modeling informed by single-cell and spatial omics data

Techniques Used: Expressing, Gene Expression, Spatial Proteomics

Patient-specific models informed by omics data (A) Metabolomics, transcriptomics, and proteomics data can be collected from a patient’s liver sample. A patient-specific genome scale metabolic model (GEM) of the liver can then be generated by integrating the transcriptomics and proteomics data with a generic GEM (i.e., Human1 or Recon2 ). Metabolic fluxes are constrained using the metabolomics data and predicted by flux balance analysis. (B) Bulk and single-cell RNA-seq data can be utilized to generate context-specific metabolic models in health and disease (i.e., liver disease). Metabolic fluxes can be predicted by flux balance analysis and significantly perturbed metabolic pathways/subsystems can be identified in health vs. disease. For example, our analysis of liver transcriptomics data from alcoholic liver disease identified significant metabolic dysregulation in the glutathione (GSH) metabolic pathway. Specifically, the metabolic flux activity of specific solute transporters (LAT1, BAT1, OATP1A2) within the GSH pathway decreased with liver disease, while healthy livers showed an increase in flux along the pathway. (C) Zone-specific hepatocyte populations can be elucidated from single-cell omics data sources. The metabolic expression for genes in the B-oxidation and gluconeogenesis pathways decreases from zone 3 to zone 1, while it increases from zone 3 to zone 1 for genes in the glycolysis and lipogenesis pathways. Marker expression for each of the zonated hepatocyte populations within the “Big” data can be utilized in conjunction with “Not So Big” experimental data (i.e., neural tracings, calcium imaging, and glycogenolytic distribution analyses) to parameterize and structure a computational model of liver innervation, calcium signaling, and glycogenolysis. Additionally, the extent of innervation to the liver can be tuned in the model to the species of interest based on physiological evidence from the literature. <xref ref-type=Figure 7 B adapted from Manchel et al., (2022). Figure 7 C adapted from Verma, Manchel et al., (2021). Created using biorender.com . " title="Patient-specific models informed by omics data (A) Metabolomics, transcriptomics, and proteomics data can be collected from a ..." property="contentUrl" width="100%" height="100%"/>
Figure Legend Snippet: Patient-specific models informed by omics data (A) Metabolomics, transcriptomics, and proteomics data can be collected from a patient’s liver sample. A patient-specific genome scale metabolic model (GEM) of the liver can then be generated by integrating the transcriptomics and proteomics data with a generic GEM (i.e., Human1 or Recon2 ). Metabolic fluxes are constrained using the metabolomics data and predicted by flux balance analysis. (B) Bulk and single-cell RNA-seq data can be utilized to generate context-specific metabolic models in health and disease (i.e., liver disease). Metabolic fluxes can be predicted by flux balance analysis and significantly perturbed metabolic pathways/subsystems can be identified in health vs. disease. For example, our analysis of liver transcriptomics data from alcoholic liver disease identified significant metabolic dysregulation in the glutathione (GSH) metabolic pathway. Specifically, the metabolic flux activity of specific solute transporters (LAT1, BAT1, OATP1A2) within the GSH pathway decreased with liver disease, while healthy livers showed an increase in flux along the pathway. (C) Zone-specific hepatocyte populations can be elucidated from single-cell omics data sources. The metabolic expression for genes in the B-oxidation and gluconeogenesis pathways decreases from zone 3 to zone 1, while it increases from zone 3 to zone 1 for genes in the glycolysis and lipogenesis pathways. Marker expression for each of the zonated hepatocyte populations within the “Big” data can be utilized in conjunction with “Not So Big” experimental data (i.e., neural tracings, calcium imaging, and glycogenolytic distribution analyses) to parameterize and structure a computational model of liver innervation, calcium signaling, and glycogenolysis. Additionally, the extent of innervation to the liver can be tuned in the model to the species of interest based on physiological evidence from the literature. Figure 7 B adapted from Manchel et al., (2022). Figure 7 C adapted from Verma, Manchel et al., (2021). Created using biorender.com .

Techniques Used: Generated, RNA Sequencing, Activity Assay, Expressing, Marker, Imaging

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Image Search Results


Single-cell transcriptome analysis of the microglia (A) UMAP shows the distribution of each subtype of microglia. (B) The sector graph shows the composition of cells in subclusters by groups. (C) Violin plot depicts the expression levels of known core signature genes for each microglia subcluster. (D) Representative immunofluorescence double staining images of NFKBIA (red), IBA1 (green), and nuclei were labeled with DAPI located in hippocampus in the NC and LPS groups. Scale bar = 75 μm or 25 μm. Quantitative analysis of the proportion of NFKBIA + cells in microglia (IBA1+) in hippocampal DG subregion. Data are shown as mean ± SEM, independent samples t-test, n = 4, ∗∗ p < 0.01. (E) Marker genes enriched KEGG pathway analyses in various microglia subpopulations. (F) GO analysis shows the top five signaling pathways across the four subpopulations, MG0, MG4, MG5 and MG7.

Journal: iScience

Article Title: Single-cell transcriptomics of neuroinflammation and cerebrovascular endothelial cells in the aged rat hippocampus

doi: 10.1016/j.isci.2025.113332

Figure Lengend Snippet: Single-cell transcriptome analysis of the microglia (A) UMAP shows the distribution of each subtype of microglia. (B) The sector graph shows the composition of cells in subclusters by groups. (C) Violin plot depicts the expression levels of known core signature genes for each microglia subcluster. (D) Representative immunofluorescence double staining images of NFKBIA (red), IBA1 (green), and nuclei were labeled with DAPI located in hippocampus in the NC and LPS groups. Scale bar = 75 μm or 25 μm. Quantitative analysis of the proportion of NFKBIA + cells in microglia (IBA1+) in hippocampal DG subregion. Data are shown as mean ± SEM, independent samples t-test, n = 4, ∗∗ p < 0.01. (E) Marker genes enriched KEGG pathway analyses in various microglia subpopulations. (F) GO analysis shows the top five signaling pathways across the four subpopulations, MG0, MG4, MG5 and MG7.

Article Snippet: Based on these results, we conducted single-cell transcriptome analysis (scRNA-seq) on aging rat hippocampus on day 3 after LPS or vehicle injection using the 10X Genomics platform to examine changes in the neuroinflammatory microenvironment ( H).

Techniques: Expressing, Immunofluorescence, Double Staining, Labeling, Marker, Protein-Protein interactions

Single-cell transcriptome analysis of the cerebral vascular endothelial cells (A–C) UMAP plot and bar plot showing the distribution of 6 subpopulations of cerebral vascular endothelial cells in the LPS and NC groups. (D) Violin plot shows the gene expression related to vascular origin (arterial, venous, and capillary), including arterial endothelial cell marker genes Fbln5, Bmx, Efnb2 , Vegfc . The venous endothelial cells highly expressed gene Nr2f and capillary endothelial cells highly expressed gene Rgcc and Slc16a1 . (E) Expression profiles of EC0 Marker genes including Mfge8, Lrg1, Lgals9, Cldn5, Ocln, Tjp1, Ddit4/Redd1, Mfsd2a are shown using the UMAP visualization approach. (F) Marker genes in the EC0 subpopulation are enriched with GO functional analysis. (G) Volcano plot depicts the DEGs at overall level of cerebral vascular endothelial cells between LPS and NC groups. DEGs (|log2(fold change)| > 1, p Value FDR <0.05, Difference = |pct.1- pct.2 | > 0.2) were colored (red for upregulated DEGs and blue for downregulated DEGs. (H and I) GO analysis shows the upregulated signaling pathway at overall level of cerebral vascular endothelial cells and EC0 subpopulation respectively.

Journal: iScience

Article Title: Single-cell transcriptomics of neuroinflammation and cerebrovascular endothelial cells in the aged rat hippocampus

doi: 10.1016/j.isci.2025.113332

Figure Lengend Snippet: Single-cell transcriptome analysis of the cerebral vascular endothelial cells (A–C) UMAP plot and bar plot showing the distribution of 6 subpopulations of cerebral vascular endothelial cells in the LPS and NC groups. (D) Violin plot shows the gene expression related to vascular origin (arterial, venous, and capillary), including arterial endothelial cell marker genes Fbln5, Bmx, Efnb2 , Vegfc . The venous endothelial cells highly expressed gene Nr2f and capillary endothelial cells highly expressed gene Rgcc and Slc16a1 . (E) Expression profiles of EC0 Marker genes including Mfge8, Lrg1, Lgals9, Cldn5, Ocln, Tjp1, Ddit4/Redd1, Mfsd2a are shown using the UMAP visualization approach. (F) Marker genes in the EC0 subpopulation are enriched with GO functional analysis. (G) Volcano plot depicts the DEGs at overall level of cerebral vascular endothelial cells between LPS and NC groups. DEGs (|log2(fold change)| > 1, p Value FDR <0.05, Difference = |pct.1- pct.2 | > 0.2) were colored (red for upregulated DEGs and blue for downregulated DEGs. (H and I) GO analysis shows the upregulated signaling pathway at overall level of cerebral vascular endothelial cells and EC0 subpopulation respectively.

Article Snippet: Based on these results, we conducted single-cell transcriptome analysis (scRNA-seq) on aging rat hippocampus on day 3 after LPS or vehicle injection using the 10X Genomics platform to examine changes in the neuroinflammatory microenvironment ( H).

Techniques: Gene Expression, Marker, Expressing, Functional Assay

Single-Cell RNA Sequencing Revealed That DP MΦs Had High Expression of Retnla Cardiac CD45 + immune cells were sorted from the sham group, 1 week post-TAC group (acute stress phase), and 9 weeks post-TAC group (chronic heart failure phase), and single-cell transcriptomic analysis was performed using the 10X Genomics platform. (A) Uniform manifold approximation and projection dimensionality reduction analysis identified that mononuclear MΦs consisted of Lyve1 hi MΦs, Lyve1 hi MHCⅡ hi MΦs, MHCⅡ hi MΦs, and monocytes after reclustering under “Lyve1score” and “MHCⅡscore” dimensions. (B) Nineteen representative differentially expressed genes are plotted as a heatmap. (C) The percentage of MΦ subsets among the total MΦs across conditions. (D) Volcano plots of differentially expressed genes across conditions including both up-regulated and down-regulated genes (minimum percentage: 0.1; logFC threshold: 0.1; adjusted P value < 0.05). Genes of interest are highlighted in red. (E) The percentage of Retlna-positive cells among the MΦ subsets detected with flow cytometry. (F) The relative expression levels of Retnla and Mgl2 in heart tissues were measured by quantitative polymerase chain reaction 3 days after diphtheria toxin injection between the sham and TAC groups (4 weeks post-TAC) using a DP MΦ–reduced model (TAC reduced). Values were analyzed by using analysis of variance with Tukey post hoc analysis. (G) Pathway enrichment analysis (gProfiler, Gene Ontology biological processes) using differentially expressed genes across conditions. ∗∗ P < 0.01; ∗∗∗ P < 0.001. avg = average; FC = fold change; mRNA = messenger RNA; other abbreviations as in <xref ref-type=Figure 1 , Figure 2 , Figure 3 . " width="100%" height="100%">

Journal: JACC: Basic to Translational Science

Article Title: TIMD4 hi MHCⅡ hi Macrophages Preserve Heart Function Through Retnla

doi: 10.1016/j.jacbts.2024.08.009

Figure Lengend Snippet: Single-Cell RNA Sequencing Revealed That DP MΦs Had High Expression of Retnla Cardiac CD45 + immune cells were sorted from the sham group, 1 week post-TAC group (acute stress phase), and 9 weeks post-TAC group (chronic heart failure phase), and single-cell transcriptomic analysis was performed using the 10X Genomics platform. (A) Uniform manifold approximation and projection dimensionality reduction analysis identified that mononuclear MΦs consisted of Lyve1 hi MΦs, Lyve1 hi MHCⅡ hi MΦs, MHCⅡ hi MΦs, and monocytes after reclustering under “Lyve1score” and “MHCⅡscore” dimensions. (B) Nineteen representative differentially expressed genes are plotted as a heatmap. (C) The percentage of MΦ subsets among the total MΦs across conditions. (D) Volcano plots of differentially expressed genes across conditions including both up-regulated and down-regulated genes (minimum percentage: 0.1; logFC threshold: 0.1; adjusted P value < 0.05). Genes of interest are highlighted in red. (E) The percentage of Retlna-positive cells among the MΦ subsets detected with flow cytometry. (F) The relative expression levels of Retnla and Mgl2 in heart tissues were measured by quantitative polymerase chain reaction 3 days after diphtheria toxin injection between the sham and TAC groups (4 weeks post-TAC) using a DP MΦ–reduced model (TAC reduced). Values were analyzed by using analysis of variance with Tukey post hoc analysis. (G) Pathway enrichment analysis (gProfiler, Gene Ontology biological processes) using differentially expressed genes across conditions. ∗∗ P < 0.01; ∗∗∗ P < 0.001. avg = average; FC = fold change; mRNA = messenger RNA; other abbreviations as in Figure 1 , Figure 2 , Figure 3 .

Article Snippet: Figure 5 Single-Cell RNA Sequencing Revealed That DP MΦs Had High Expression of Retnla Cardiac CD45 + immune cells were sorted from the sham group, 1 week post-TAC group (acute stress phase), and 9 weeks post-TAC group (chronic heart failure phase), and single-cell transcriptomic analysis was performed using the 10X Genomics platform. (A) Uniform manifold approximation and projection dimensionality reduction analysis identified that mononuclear MΦs consisted of Lyve1 hi MΦs, Lyve1 hi MHCII hi MΦs, MHCII hi MΦs, and monocytes after reclustering under “Lyve1score” and “MHCIIscore” dimensions. (B) Nineteen representative differentially expressed genes are plotted as a heatmap. (C) The percentage of MΦ subsets among the total MΦs across conditions. (D) Volcano plots of differentially expressed genes across conditions including both up-regulated and down-regulated genes (minimum percentage: 0.1; logFC threshold: 0.1; adjusted P value < 0.05).

Techniques: RNA Sequencing, Expressing, Flow Cytometry, Real-time Polymerase Chain Reaction, Injection