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<t>CD8</t> + T cytotoxic cells are the predominant subset within the T and NK cell compartment in the colon of chronically infected mice (A) Uniform manifold approximation and projection (UMAP) plot showing nine T and NK cell subclusters. Each point represents a single cell. (B) Bar graph depicts the relative percentages of each cell subtype in naive and infected mice. (C) Representative flow cytometry plots of CD8 + T cells in naive (left) and infected mice (right). Cells were gated on live, singlets, CD3 + cells. (D) Violin plot shows the percentage of CD8 + T cells in naive and infected mice. (E) Representative flow cytometry plots of T follicular helper cells in naive (left) and infected mice (right). Cells were gated on live, singlets, CD3 + CD4 + cells. (F) Violin plot shows the percentage of PD-1 + CXCR4 + T follicular helper cells in naive and chronically infected mice. Data are representative of two independent experiments with a total of 6 (in D) or 4 (in F) mice per group. In (D and F), violin plots show the distribution of values for each group. Individual points represent biological replicates. Large dashed horizontal lines indicate the median. Statistical significance was determined by an unpaired t test. ∗∗∗: p < 0.001; ns: not significant.

Cd8a Ly 2 Microbeads, supplied by Miltenyi Biotec, used in various techniques. Bioz Stars score: 96/100, based on 267 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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1) Product Images from "CCL signaling drives T Cell–Macrophage crosstalk in the mouse colon during chronic Trypanosoma cruzi infection"

Article Title: CCL signaling drives T Cell–Macrophage crosstalk in the mouse colon during chronic Trypanosoma cruzi infection

Journal: iScience

doi: 10.1016/j.isci.2026.116611

CD8 + T cytotoxic cells are the predominant subset within the T and NK cell compartment in the colon of chronically infected mice (A) Uniform manifold approximation and projection (UMAP) plot showing nine T and NK cell subclusters. Each point represents a single cell. (B) Bar graph depicts the relative percentages of each cell subtype in naive and infected mice. (C) Representative flow cytometry plots of CD8 + T cells in naive (left) and infected mice (right). Cells were gated on live, singlets, CD3 + cells. (D) Violin plot shows the percentage of CD8 + T cells in naive and infected mice. (E) Representative flow cytometry plots of T follicular helper cells in naive (left) and infected mice (right). Cells were gated on live, singlets, CD3 + CD4 + cells. (F) Violin plot shows the percentage of PD-1 + CXCR4 + T follicular helper cells in naive and chronically infected mice. Data are representative of two independent experiments with a total of 6 (in D) or 4 (in F) mice per group. In (D and F), violin plots show the distribution of values for each group. Individual points represent biological replicates. Large dashed horizontal lines indicate the median. Statistical significance was determined by an unpaired t test. ∗∗∗: p < 0.001; ns: not significant.

Figure Legend Snippet: CD8 + T cytotoxic cells are the predominant subset within the T and NK cell compartment in the colon of chronically infected mice (A) Uniform manifold approximation and projection (UMAP) plot showing nine T and NK cell subclusters. Each point represents a single cell. (B) Bar graph depicts the relative percentages of each cell subtype in naive and infected mice. (C) Representative flow cytometry plots of CD8 + T cells in naive (left) and infected mice (right). Cells were gated on live, singlets, CD3 + cells. (D) Violin plot shows the percentage of CD8 + T cells in naive and infected mice. (E) Representative flow cytometry plots of T follicular helper cells in naive (left) and infected mice (right). Cells were gated on live, singlets, CD3 + CD4 + cells. (F) Violin plot shows the percentage of PD-1 + CXCR4 + T follicular helper cells in naive and chronically infected mice. Data are representative of two independent experiments with a total of 6 (in D) or 4 (in F) mice per group. In (D and F), violin plots show the distribution of values for each group. Individual points represent biological replicates. Large dashed horizontal lines indicate the median. Statistical significance was determined by an unpaired t test. ∗∗∗: p < 0.001; ns: not significant.

Techniques Used: Infection, Single Cell, Flow Cytometry

CD8 + cytotoxic T cells contribute as central mediators within the CCL signaling network (A) Violin plots show the distribution and density of CCL5 (left) and CCR5 (right) expression across T and NK cell subsets, as well as macrophages, in the colon of naive and chronically infected mice. Wider sections of the violin indicate a higher proportion of cells expressing CCL5 or CCR5 at that level. Data were generated from CellChat-guided analysis of scRNA-seq profiles. (B) Representative flow cytometry plots show CD8 + CCR5 + T cells in the colon of naive (upper panel) and chronically infected mice (bottom panel). Cells were gated on live, singlets, and CD3 + cells. (C) Representative flow cytometry plots show F4/80 + CCR5 + T cells in naive (upper panel) and chronically infected mice (bottom panel). Cells were gated on live, singlets, and CD45 + cells. (D) Violin plot shows the frequency of CD8 + CCR5 + T cells in naive and chronically infected mice. Data are representative of two independent experiments ( n = 4 mice per group). (E) mRNA quantification of Ccl5 and Ccr5 by qRT-PCR in naive and chronically infected mice. The plot shows log 2 fold changes (FC) in gene expression determined by the ΔC t method with normalization to GAPDH. The horizontal line indicates the median value for each group, with individual data points plotted. CD8 + T cells were purified from the lamina propria of naive and chronically infected mice using magnetic bead–based separation prior to RNA extraction. Data are from three independent experiments. (F) Violin plot shows the frequency of F4/80 + CCR5 + T cells in the colon of naive and chronically infected mice. Data are representative of two independent experiments ( n = 3 mice per group). In (D and F), violin plots show the distribution of values for each group. Individual points represent biological replicates. Large dashed horizontal lines indicate the median. Statistical significance was determined by an unpaired t test. ∗∗: p < 0.01; ns: not significant.

Figure Legend Snippet: CD8 + cytotoxic T cells contribute as central mediators within the CCL signaling network (A) Violin plots show the distribution and density of CCL5 (left) and CCR5 (right) expression across T and NK cell subsets, as well as macrophages, in the colon of naive and chronically infected mice. Wider sections of the violin indicate a higher proportion of cells expressing CCL5 or CCR5 at that level. Data were generated from CellChat-guided analysis of scRNA-seq profiles. (B) Representative flow cytometry plots show CD8 + CCR5 + T cells in the colon of naive (upper panel) and chronically infected mice (bottom panel). Cells were gated on live, singlets, and CD3 + cells. (C) Representative flow cytometry plots show F4/80 + CCR5 + T cells in naive (upper panel) and chronically infected mice (bottom panel). Cells were gated on live, singlets, and CD45 + cells. (D) Violin plot shows the frequency of CD8 + CCR5 + T cells in naive and chronically infected mice. Data are representative of two independent experiments ( n = 4 mice per group). (E) mRNA quantification of Ccl5 and Ccr5 by qRT-PCR in naive and chronically infected mice. The plot shows log 2 fold changes (FC) in gene expression determined by the ΔC t method with normalization to GAPDH. The horizontal line indicates the median value for each group, with individual data points plotted. CD8 + T cells were purified from the lamina propria of naive and chronically infected mice using magnetic bead–based separation prior to RNA extraction. Data are from three independent experiments. (F) Violin plot shows the frequency of F4/80 + CCR5 + T cells in the colon of naive and chronically infected mice. Data are representative of two independent experiments ( n = 3 mice per group). In (D and F), violin plots show the distribution of values for each group. Individual points represent biological replicates. Large dashed horizontal lines indicate the median. Statistical significance was determined by an unpaired t test. ∗∗: p < 0.01; ns: not significant.

Techniques Used: Expressing, Infection, Generated, Flow Cytometry, Quantitative RT-PCR, Gene Expression, Purification, RNA Extraction

CD8 + cytotoxic T cell–macrophage interactions likely shape colonic immune homeostasis during chronic T. cruzi infection (A) Volcano plot showing differentially expressed genes (DEGs) in lamina propria CD8 + cytotoxic T cells from infected mice compared with naive controls. Red dots depict upregulated genes, blue dots indicate downregulated genes, and gray dots represent genes with a non-significant change in expression. Genes with log 2 fold change ≥1.5, and p < 0.05 were considered significant. (B) Top five differentially regulated canonical pathways in lamina propria CD8 + cytotoxic T cells from infected mice, as predicted by ingenuity pathway analysis (IPA). Bars represent −log ( p value); red indicates pathway activation and blue indicates pathway inhibition. (C) Top 10 upregulated genes associated with the IL-4/IL-13 signaling pathway (left) and the pathogen-induced cytokine storm (PICS) pathway (right) in CD8 + cytotoxic T cells. (D) Volcano plot of DEGs in lamina propria macrophages from infected mice compared with naive controls, displayed as in (A). (E) Top five differentially regulated canonical pathways in lamina propria macrophages from infected mice, as predicted by IPA, displayed as in (B). (F) Top 10 upregulated genes associated with the S100 protein family signaling pathway (left) and the neutrophil degranulation pathway (right) in macrophages. In (C and F), bars indicate log 2 fold change between infected and naive mice.

Figure Legend Snippet: CD8 + cytotoxic T cell–macrophage interactions likely shape colonic immune homeostasis during chronic T. cruzi infection (A) Volcano plot showing differentially expressed genes (DEGs) in lamina propria CD8 + cytotoxic T cells from infected mice compared with naive controls. Red dots depict upregulated genes, blue dots indicate downregulated genes, and gray dots represent genes with a non-significant change in expression. Genes with log 2 fold change ≥1.5, and p < 0.05 were considered significant. (B) Top five differentially regulated canonical pathways in lamina propria CD8 + cytotoxic T cells from infected mice, as predicted by ingenuity pathway analysis (IPA). Bars represent −log ( p value); red indicates pathway activation and blue indicates pathway inhibition. (C) Top 10 upregulated genes associated with the IL-4/IL-13 signaling pathway (left) and the pathogen-induced cytokine storm (PICS) pathway (right) in CD8 + cytotoxic T cells. (D) Volcano plot of DEGs in lamina propria macrophages from infected mice compared with naive controls, displayed as in (A). (E) Top five differentially regulated canonical pathways in lamina propria macrophages from infected mice, as predicted by IPA, displayed as in (B). (F) Top 10 upregulated genes associated with the S100 protein family signaling pathway (left) and the neutrophil degranulation pathway (right) in macrophages. In (C and F), bars indicate log 2 fold change between infected and naive mice.

Techniques Used: Infection, Expressing, Activation Assay, Inhibition

Proposed model of the immune response mechanisms to Trypanosoma cruzi in the mouse colon, integrating our findings with prior studies ① Infected smooth muscle cells release trypomastigotes into the surrounding colonic tissue. ② Trypomastigotes are phagocytosed by macrophages. ③ After 18–24 hs post-internalization, amastigotes are released into the cytoplasm, where they replicate and synthesize proteins that are presented on the macrophage surface. ④ CD8 + and CD4 + T cells recognize T. cruzi peptides presented by MHC complexes. ⑤ Upon activation, CD8 + T cells secrete granzyme A and multiple cytokines. ⑥ Granzyme A -containing granules may enter parasite-infected smooth muscle cells through pores formed by perforin-1 (PRF1; secreted by NK cells), contributing to cell death. ⑦ Tumor necrosis factor (TNF) may promote macrophage polarization to an M1 phenotype by inducing the expression of inducible nitric oxide synthase (NOS2). This enzyme subsequently oxidizes arginine to produce nitric oxide, which may contribute to parasite killing. ⑧ Activated CD4 + T cells can differentiate into Th and Tfh cells that produce Interleukin-4 (IL-4) and Interleukin-13 (IL-13) [⑨], which in turn induce M2 macrophage polarization. ⑩ C-C Motif Ligand 5 (CCL5) could further support M2 macrophage polarization via arginase I (ARG1) upregulation, promoting polyamines associated with parasite multiplication and persistence. ⑪ Amastigotes differentiate into trypomastigotes, completing the cycle by infecting naive smooth muscle cells.

Figure Legend Snippet: Proposed model of the immune response mechanisms to Trypanosoma cruzi in the mouse colon, integrating our findings with prior studies ① Infected smooth muscle cells release trypomastigotes into the surrounding colonic tissue. ② Trypomastigotes are phagocytosed by macrophages. ③ After 18–24 hs post-internalization, amastigotes are released into the cytoplasm, where they replicate and synthesize proteins that are presented on the macrophage surface. ④ CD8 + and CD4 + T cells recognize T. cruzi peptides presented by MHC complexes. ⑤ Upon activation, CD8 + T cells secrete granzyme A and multiple cytokines. ⑥ Granzyme A -containing granules may enter parasite-infected smooth muscle cells through pores formed by perforin-1 (PRF1; secreted by NK cells), contributing to cell death. ⑦ Tumor necrosis factor (TNF) may promote macrophage polarization to an M1 phenotype by inducing the expression of inducible nitric oxide synthase (NOS2). This enzyme subsequently oxidizes arginine to produce nitric oxide, which may contribute to parasite killing. ⑧ Activated CD4 + T cells can differentiate into Th and Tfh cells that produce Interleukin-4 (IL-4) and Interleukin-13 (IL-13) [⑨], which in turn induce M2 macrophage polarization. ⑩ C-C Motif Ligand 5 (CCL5) could further support M2 macrophage polarization via arginase I (ARG1) upregulation, promoting polyamines associated with parasite multiplication and persistence. ⑪ Amastigotes differentiate into trypomastigotes, completing the cycle by infecting naive smooth muscle cells.

Techniques Used: Infection, Activation Assay, Expressing

Positive Control:

Article Title: SPNS2 exports sphingosine-1-phosphate and imports glucose.
Article Snippet: Cells were washed and resuspended in flow buffer for analysis with a BD LSRFortessa X-20 Cell Analyzer (BD Bioscience) equipped with BD FACSDiva 8.0 software for acquisition. .. As a positive control, primary T lymphocytes from WT AR TI CL E IN P RE SS animals were isolated from the spleen with a combination of CD4 (L3T4) and CD8a (Ly-2) MicroBeads (#130-117-043, 130-117-044, Miltenyi Biotec) and magnetic-activated cell sorting. .. Isolated T lymphocytes were left untreated or stimulated with surface-coated monoclonal antiCD3ε (5 μg/mL diluted in PBS, incubated for 2 h at 37°C for immobilization; #100301, BioLegend) and 1.7 μg/mL monoclonal soluble anti-CD28 (#102101, BioLegend) for 24 h as described 69.

Article Title: SPNS2 exports sphingosine-1-phosphate and imports glucose
Article Snippet: Cells were washed and resuspended in flow buffer for analysis with a BD LSRFortessa X-20 Cell Analyzer (BD Bioscience) equipped with BD FACSDiva 8.0 software for acquisition. .. As a positive control, primary T lymphocytes from WT animals were isolated from the spleen with a combination of CD4 (L3T4) and CD8a (Ly-2) MicroBeads (#130-117-043, 130-117-044, Miltenyi Biotec) and magnetic-activated cell sorting. .. Isolated T lymphocytes were left untreated or stimulated with surface-coated monoclonal anti-CD3ε (5 μg/mL diluted in PBS, incubated for 2 h at 37 °C for immobilization; #100301, BioLegend) and 1.7 μg/mL monoclonal soluble anti-CD28 (#102101, BioLegend) for 24 h as described .

Isolation:

Article Title: Low-dose radiotherapy synergizes with PD-1 blockade to achieve durable survival in advanced NSCLC through antitumor neutrophil programming
Article Snippet: Neutrophils were isolated from C57BL/6 and CD45.1 bone marrow using the Neutrophil Isolation Kit (Miltenyi Biotec, Cat# 130-097-658) and LS columns (Miltenyi Biotec, Cat# 130-042-401) per instructions. .. CD8 + T cells were isolated from C57BL/6 spleens using CD8a (Ly-2) MicroBeads (Miltenyi Biotec, Cat# 130-117-044) and LS columns (Miltenyi Biotec, Cat# 130-042-401). .. Sorted neutrophils were cultured with IFN-γ (10 ng/mL; PeproTech, Cat# 315-05-500UG) and GM-CSF (0.05 ng/mL; PeproTech, Cat# 315-03-20UG) for 24 h. To maintain neutrophil activity, LPS (Sigma-Aldrich; 100 ng/mL) was added.

Article Title: Soluble CD155 immune complexes reprogram DNAM-1 signaling to potentiate antitumor immunity
Article Snippet: For the stimulation of primary CD8 + T cells, 96-well plates were co-coated overnight with 500 ng/well of anti-sCD155 mAb or an isotype control, alongside indicated concentrations (0 to 30 ng/well) of anti-CD3e mAb (clone 145-2C11, #100340, BioLegend). .. Primary CD8 + T cells were isolated from the spleens of male C57BL/6J WT mice and purified using CD8a (Ly-2) MicroBeads (#130-117-044, Miltenyi Biotec) and LS columns (#130-042-401, Miltenyi Biotec) according to the manufacturer’s instructions. ..

Article Title: Pharmacologic DPP-4 inhibition promotes CD8⁺ T cell metabolic fitness to enhance anti-tumor activity
Article Snippet: .. Mouse CD8 + T-cells were isolated from freshly harvested spleens of C57BL/6 mice using CD8a (Ly-2) MicroBeads (Miltenyi #130-114-044), following manufacturer’s instructions. .. After isolation, T cells were stained with 10 μM 5-(and 6)-Carboxyfluorescein diacetate succinimidyl ester (CFSE, Biolegend #423801) in the dark for 5 minutes at 37°C and reaction was quenched with ice-cold RPMI containing 10% FBS.

FACS:

Purification:

Incubation:

Article Title: Extracellular vesicles from chemotherapy-induced senescent tumor cells reprogram hepatic phospholipid metabolism to promote pancreatic cancer liver metastasis.
Article Snippet: .. Cells were resuspended in autoMACS Running Buffer (Miltenyi, 130-091-221), adjusted to 1×10 7 cells/100 μL, incubated with CD8a (Ly-2) MicroBeads (Miltenyi, 130-117-044; 10 μL/1×10 7 cells) for 15 min at 4 °C, washed, and selected on an autoMACS separator. ..

Image Search Results

Journal: iScience

Article Title: CCL signaling drives T Cell–Macrophage crosstalk in the mouse colon during chronic Trypanosoma cruzi infection

doi: 10.1016/j.isci.2026.116611

Figure Lengend Snippet: CD8 + T cytotoxic cells are the predominant subset within the T and NK cell compartment in the colon of chronically infected mice (A) Uniform manifold approximation and projection (UMAP) plot showing nine T and NK cell subclusters. Each point represents a single cell. (B) Bar graph depicts the relative percentages of each cell subtype in naive and infected mice. (C) Representative flow cytometry plots of CD8 + T cells in naive (left) and infected mice (right). Cells were gated on live, singlets, CD3 + cells. (D) Violin plot shows the percentage of CD8 + T cells in naive and infected mice. (E) Representative flow cytometry plots of T follicular helper cells in naive (left) and infected mice (right). Cells were gated on live, singlets, CD3 + CD4 + cells. (F) Violin plot shows the percentage of PD-1 + CXCR4 + T follicular helper cells in naive and chronically infected mice. Data are representative of two independent experiments with a total of 6 (in D) or 4 (in F) mice per group. In (D and F), violin plots show the distribution of values for each group. Individual points represent biological replicates. Large dashed horizontal lines indicate the median. Statistical significance was determined by an unpaired t test. ∗∗∗: p < 0.001; ns: not significant.

Article Snippet: CD8a (Ly-2) Microbeads , Miltenyi Biotec , Cat-130-117-044.

Techniques: Infection, Single Cell, Flow Cytometry

Journal: iScience

Article Title: CCL signaling drives T Cell–Macrophage crosstalk in the mouse colon during chronic Trypanosoma cruzi infection

doi: 10.1016/j.isci.2026.116611

Figure Lengend Snippet: CD8 + cytotoxic T cells contribute as central mediators within the CCL signaling network (A) Violin plots show the distribution and density of CCL5 (left) and CCR5 (right) expression across T and NK cell subsets, as well as macrophages, in the colon of naive and chronically infected mice. Wider sections of the violin indicate a higher proportion of cells expressing CCL5 or CCR5 at that level. Data were generated from CellChat-guided analysis of scRNA-seq profiles. (B) Representative flow cytometry plots show CD8 + CCR5 + T cells in the colon of naive (upper panel) and chronically infected mice (bottom panel). Cells were gated on live, singlets, and CD3 + cells. (C) Representative flow cytometry plots show F4/80 + CCR5 + T cells in naive (upper panel) and chronically infected mice (bottom panel). Cells were gated on live, singlets, and CD45 + cells. (D) Violin plot shows the frequency of CD8 + CCR5 + T cells in naive and chronically infected mice. Data are representative of two independent experiments ( n = 4 mice per group). (E) mRNA quantification of Ccl5 and Ccr5 by qRT-PCR in naive and chronically infected mice. The plot shows log 2 fold changes (FC) in gene expression determined by the ΔC t method with normalization to GAPDH. The horizontal line indicates the median value for each group, with individual data points plotted. CD8 + T cells were purified from the lamina propria of naive and chronically infected mice using magnetic bead–based separation prior to RNA extraction. Data are from three independent experiments. (F) Violin plot shows the frequency of F4/80 + CCR5 + T cells in the colon of naive and chronically infected mice. Data are representative of two independent experiments ( n = 3 mice per group). In (D and F), violin plots show the distribution of values for each group. Individual points represent biological replicates. Large dashed horizontal lines indicate the median. Statistical significance was determined by an unpaired t test. ∗∗: p < 0.01; ns: not significant.

Article Snippet: CD8a (Ly-2) Microbeads , Miltenyi Biotec , Cat-130-117-044.

Techniques: Expressing, Infection, Generated, Flow Cytometry, Quantitative RT-PCR, Gene Expression, Purification, RNA Extraction

Journal: iScience

Article Title: CCL signaling drives T Cell–Macrophage crosstalk in the mouse colon during chronic Trypanosoma cruzi infection

doi: 10.1016/j.isci.2026.116611

Figure Lengend Snippet: CD8 + cytotoxic T cell–macrophage interactions likely shape colonic immune homeostasis during chronic T. cruzi infection (A) Volcano plot showing differentially expressed genes (DEGs) in lamina propria CD8 + cytotoxic T cells from infected mice compared with naive controls. Red dots depict upregulated genes, blue dots indicate downregulated genes, and gray dots represent genes with a non-significant change in expression. Genes with log 2 fold change ≥1.5, and p < 0.05 were considered significant. (B) Top five differentially regulated canonical pathways in lamina propria CD8 + cytotoxic T cells from infected mice, as predicted by ingenuity pathway analysis (IPA). Bars represent −log ( p value); red indicates pathway activation and blue indicates pathway inhibition. (C) Top 10 upregulated genes associated with the IL-4/IL-13 signaling pathway (left) and the pathogen-induced cytokine storm (PICS) pathway (right) in CD8 + cytotoxic T cells. (D) Volcano plot of DEGs in lamina propria macrophages from infected mice compared with naive controls, displayed as in (A). (E) Top five differentially regulated canonical pathways in lamina propria macrophages from infected mice, as predicted by IPA, displayed as in (B). (F) Top 10 upregulated genes associated with the S100 protein family signaling pathway (left) and the neutrophil degranulation pathway (right) in macrophages. In (C and F), bars indicate log 2 fold change between infected and naive mice.

Article Snippet: CD8a (Ly-2) Microbeads , Miltenyi Biotec , Cat-130-117-044.

Techniques: Infection, Expressing, Activation Assay, Inhibition

Journal: iScience

Article Title: CCL signaling drives T Cell–Macrophage crosstalk in the mouse colon during chronic Trypanosoma cruzi infection

doi: 10.1016/j.isci.2026.116611

Figure Lengend Snippet: Proposed model of the immune response mechanisms to Trypanosoma cruzi in the mouse colon, integrating our findings with prior studies ① Infected smooth muscle cells release trypomastigotes into the surrounding colonic tissue. ② Trypomastigotes are phagocytosed by macrophages. ③ After 18–24 hs post-internalization, amastigotes are released into the cytoplasm, where they replicate and synthesize proteins that are presented on the macrophage surface. ④ CD8 + and CD4 + T cells recognize T. cruzi peptides presented by MHC complexes. ⑤ Upon activation, CD8 + T cells secrete granzyme A and multiple cytokines. ⑥ Granzyme A -containing granules may enter parasite-infected smooth muscle cells through pores formed by perforin-1 (PRF1; secreted by NK cells), contributing to cell death. ⑦ Tumor necrosis factor (TNF) may promote macrophage polarization to an M1 phenotype by inducing the expression of inducible nitric oxide synthase (NOS2). This enzyme subsequently oxidizes arginine to produce nitric oxide, which may contribute to parasite killing. ⑧ Activated CD4 + T cells can differentiate into Th and Tfh cells that produce Interleukin-4 (IL-4) and Interleukin-13 (IL-13) [⑨], which in turn induce M2 macrophage polarization. ⑩ C-C Motif Ligand 5 (CCL5) could further support M2 macrophage polarization via arginase I (ARG1) upregulation, promoting polyamines associated with parasite multiplication and persistence. ⑪ Amastigotes differentiate into trypomastigotes, completing the cycle by infecting naive smooth muscle cells.

Article Snippet: CD8a (Ly-2) Microbeads , Miltenyi Biotec , Cat-130-117-044.

Techniques: Infection, Activation Assay, Expressing

Single-cell RNA sequencing (scRNA-seq) analysis of the tumor microenvironment (TME) in TNBC patients. (A) UMAP visualization of major cell populations within TNBC tumors. (B) Comparative analysis of immune cell frequencies in the TME of TNBC patients with and without chemotherapy. (C) UMAP visualization of macrophages within TNBC tumors. (D) Changes in macrophage subtype frequencies in the TME of TNBC patients with and without chemotherapy. (E) Kaplan–Meier survival analysis of TNBC patients from the TCGA database stratified by CD163 high CD8A low and CD163 low CD8A high expression ( P = 0.016). (F) Kaplan–Meier survival analysis of TNBC patients from the TCGA database stratified by ARG1 high CD8A low and ARG1 low CD8A high expression ( P = 0.049). (G) Representative immunohistochemical (IHC) staining of CD8 and CD163 in tumor tissue microarrays from TNBC patients. Scale bar = 100 μm. (H) Correlation analysis of CD8 and CD163 expression in chemotherapy-treated versus untreated TNBC patients (Patient 18,383: untreated; Patient 15,840: treated). (I) Two major clinical chemotherapies in the 4T1 murine triple negative breast cancer model time schedule. (J) Tumor volume analysis (K), Tumor weight (L), CD8/CD45, and (M) M1/M2 in TME. Data are presented as mean ± SEM. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001, ∗∗∗∗ P < 0.0001.

Journal: Acta Pharmaceutica Sinica. B

Article Title: Astragalus-derived nano-agonist potentiates chemotherapy by reducing tumor-suppressive macrophages

doi: 10.1016/j.apsb.2026.03.051

Figure Lengend Snippet: Single-cell RNA sequencing (scRNA-seq) analysis of the tumor microenvironment (TME) in TNBC patients. (A) UMAP visualization of major cell populations within TNBC tumors. (B) Comparative analysis of immune cell frequencies in the TME of TNBC patients with and without chemotherapy. (C) UMAP visualization of macrophages within TNBC tumors. (D) Changes in macrophage subtype frequencies in the TME of TNBC patients with and without chemotherapy. (E) Kaplan–Meier survival analysis of TNBC patients from the TCGA database stratified by CD163 high CD8A low and CD163 low CD8A high expression ( P = 0.016). (F) Kaplan–Meier survival analysis of TNBC patients from the TCGA database stratified by ARG1 high CD8A low and ARG1 low CD8A high expression ( P = 0.049). (G) Representative immunohistochemical (IHC) staining of CD8 and CD163 in tumor tissue microarrays from TNBC patients. Scale bar = 100 μm. (H) Correlation analysis of CD8 and CD163 expression in chemotherapy-treated versus untreated TNBC patients (Patient 18,383: untreated; Patient 15,840: treated). (I) Two major clinical chemotherapies in the 4T1 murine triple negative breast cancer model time schedule. (J) Tumor volume analysis (K), Tumor weight (L), CD8/CD45, and (M) M1/M2 in TME. Data are presented as mean ± SEM. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001, ∗∗∗∗ P < 0.0001.

Article Snippet: CD8 + T lymphocytes were extracted from the spleen of BALB/c mice with the CD8a microbeads kit (Miltenyi, 130-117-044, Bergisch Gladbach, Germany).

Techniques: Single Cell, RNA Sequencing, Expressing, Immunohistochemical staining, Immunohistochemistry

Analysis of T lymphocyte phenotypes and macrophage subtypes in TME. (A) Proportion of CD45 cells in live cells ( n = 6 per group). (B) Ratio of macrophages to CD45 + T cells ( n = 5–6 per group). (C) Proportion of CD86 high CD206 low macrophages in TAMs ( n = 6 per group). (D) Proportion of CD86 low CD206 high macrophages among TAMs ( n = 6 per group). (E) Ratio of M1-like to M2-like macrophages ( n = 4 per group). (F) Proportion of CD3 lymphocytes in CD45 cells ( n = 5 per group). (G) Ratio of CD8 + /CD3 + T lymphocytes ( n = 5–7 per group). (H) Ratio of CD8 + to Treg ( n = 5–6 per group). (I) Flow cytometry analysis of PD-1 + CD8 + T, (J) PD-1 + CD4 + T cells, and (K) TIM3 + CD4 + T in the tumor ( n = 4–7 per group). ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001, ∗∗∗∗ P < 0.0001. Data are presented as mean ± SEM and analyzed by one-way ANOVA.

Journal: Acta Pharmaceutica Sinica. B

Article Title: Astragalus-derived nano-agonist potentiates chemotherapy by reducing tumor-suppressive macrophages

doi: 10.1016/j.apsb.2026.03.051

Figure Lengend Snippet: Analysis of T lymphocyte phenotypes and macrophage subtypes in TME. (A) Proportion of CD45 cells in live cells ( n = 6 per group). (B) Ratio of macrophages to CD45 + T cells ( n = 5–6 per group). (C) Proportion of CD86 high CD206 low macrophages in TAMs ( n = 6 per group). (D) Proportion of CD86 low CD206 high macrophages among TAMs ( n = 6 per group). (E) Ratio of M1-like to M2-like macrophages ( n = 4 per group). (F) Proportion of CD3 lymphocytes in CD45 cells ( n = 5 per group). (G) Ratio of CD8 + /CD3 + T lymphocytes ( n = 5–7 per group). (H) Ratio of CD8 + to Treg ( n = 5–6 per group). (I) Flow cytometry analysis of PD-1 + CD8 + T, (J) PD-1 + CD4 + T cells, and (K) TIM3 + CD4 + T in the tumor ( n = 4–7 per group). ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001, ∗∗∗∗ P < 0.0001. Data are presented as mean ± SEM and analyzed by one-way ANOVA.

Article Snippet: CD8 + T lymphocytes were extracted from the spleen of BALB/c mice with the CD8a microbeads kit (Miltenyi, 130-117-044, Bergisch Gladbach, Germany).

Techniques: Flow Cytometry

Analysis of T lymphocyte-related cytotoxic functions in the TME of 4T1 triple-negative breast cancer (TNBC) bearing mice treated with Vehicle, ADNPs, Cisplatin, or ADNPs-Cis. Proportion of (A) IFN- γ + CD8 + , (B) Granzyme B + CD8 + , (C) TNF- α + CD8 + ( n = 4–5 for each group). (D) Ki67 + CD8 + ( n = 5–6 for each group) in CD8 + T Cells. (E) HE staining analysis of CD8 expression in the tumor and IOD analysis ( n = 3, Scale bar = 50 μm). (F) IFN- γ + CD4 + ( n = 4–5 for each group). (G) Granzyme B + CD4 + ( n = 5 for each group). (H) TNF- α + CD4 + ( n = 5–6 for each group) among CD4 + T cells. (I) Schematic representation of the co-culture system for macrophages and CD8 + T lymphocytes. (J) ADNPs treated M2-like BMDMs reversed the proliferation of CD8 + T cells and (K) the statistics. ( n = 4 per group). ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001, ∗∗∗∗ P < 0.0001. Data are presented as mean ± SEM and analyzed by one-way ANOVA.

Journal: Acta Pharmaceutica Sinica. B

Article Title: Astragalus-derived nano-agonist potentiates chemotherapy by reducing tumor-suppressive macrophages

doi: 10.1016/j.apsb.2026.03.051

Figure Lengend Snippet: Analysis of T lymphocyte-related cytotoxic functions in the TME of 4T1 triple-negative breast cancer (TNBC) bearing mice treated with Vehicle, ADNPs, Cisplatin, or ADNPs-Cis. Proportion of (A) IFN- γ + CD8 + , (B) Granzyme B + CD8 + , (C) TNF- α + CD8 + ( n = 4–5 for each group). (D) Ki67 + CD8 + ( n = 5–6 for each group) in CD8 + T Cells. (E) HE staining analysis of CD8 expression in the tumor and IOD analysis ( n = 3, Scale bar = 50 μm). (F) IFN- γ + CD4 + ( n = 4–5 for each group). (G) Granzyme B + CD4 + ( n = 5 for each group). (H) TNF- α + CD4 + ( n = 5–6 for each group) among CD4 + T cells. (I) Schematic representation of the co-culture system for macrophages and CD8 + T lymphocytes. (J) ADNPs treated M2-like BMDMs reversed the proliferation of CD8 + T cells and (K) the statistics. ( n = 4 per group). ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001, ∗∗∗∗ P < 0.0001. Data are presented as mean ± SEM and analyzed by one-way ANOVA.

Article Snippet: CD8 + T lymphocytes were extracted from the spleen of BALB/c mice with the CD8a microbeads kit (Miltenyi, 130-117-044, Bergisch Gladbach, Germany).

Techniques: Staining, Expressing, Co-Culture Assay

ADNPs reprogram M2-like macrophages into an M1-like phenotype. (A) RT-PCR analysis of IL-6 , tnfα , cxcl9 , inos , tlr2 , and cd8 6 mRNA expression in M2-like macrophages treated with ADNPs for 6 and 12 h in vitro ( n = 3 per group). (B) ROS level in supernatants of BMDMs was detected by FACS in vitro . (C) Mean fluorescence intensity analysis of CD206, CD80, and CD86 of BMDMs in vitro ( n = 3 per group). (D) Concentration of TNF- α , IL-6, IL-10, and IL-8 in the supernatant of BMDMs treated with ADNPs in vitro ( n = 3–6 per group). ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001, ∗∗∗∗ P < 0.0001. Data are presented as mean ± SEM and analyzed by one-way ANOVA or t test.

Journal: Acta Pharmaceutica Sinica. B

Article Title: Astragalus-derived nano-agonist potentiates chemotherapy by reducing tumor-suppressive macrophages

doi: 10.1016/j.apsb.2026.03.051

Figure Lengend Snippet: ADNPs reprogram M2-like macrophages into an M1-like phenotype. (A) RT-PCR analysis of IL-6 , tnfα , cxcl9 , inos , tlr2 , and cd8 6 mRNA expression in M2-like macrophages treated with ADNPs for 6 and 12 h in vitro ( n = 3 per group). (B) ROS level in supernatants of BMDMs was detected by FACS in vitro . (C) Mean fluorescence intensity analysis of CD206, CD80, and CD86 of BMDMs in vitro ( n = 3 per group). (D) Concentration of TNF- α , IL-6, IL-10, and IL-8 in the supernatant of BMDMs treated with ADNPs in vitro ( n = 3–6 per group). ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001, ∗∗∗∗ P < 0.0001. Data are presented as mean ± SEM and analyzed by one-way ANOVA or t test.

Article Snippet: CD8 + T lymphocytes were extracted from the spleen of BALB/c mice with the CD8a microbeads kit (Miltenyi, 130-117-044, Bergisch Gladbach, Germany).

Techniques: Reverse Transcription Polymerase Chain Reaction, Expressing, In Vitro, Fluorescence, Concentration Assay

Review

cd8a ly 2 microbeads (Miltenyi Biotec)

Structured Review

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1) Product Images from "CCL signaling drives T Cell–Macrophage crosstalk in the mouse colon during chronic Trypanosoma cruzi infection"

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