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anti trem1  (R&D Systems)


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    Structured Review

    R&D Systems anti trem1
    Anti Trem1, supplied by R&D Systems, used in various techniques. Bioz Stars score: 94/100, based on 9 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/anti+trem1/pm41782012-77-25-26?v=R%26D+Systems
    Average 94 stars, based on 9 article reviews
    anti trem1 - by Bioz Stars, 2026-07
    94/100 stars

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    Bioss pe cy7 anti mouse trem1
    scRNA-seq reveals a new MES-MDM in patients with GBM. (A) T-SNE plots showing unsupervised clusters of nine cell types superclusters. The nine superclusters are: cancer cell, monocyte-derived macrophages (MDM), monocyte, microglial Cells (MGcells), endothelial cells (ECs), lymphocytes, oligodendrocyte, stromal cells (SCs), and neutrophils. Dots represent individual cells, and colors represent different cell populations. (B) The SCENIC analysis identified five transcription factor (TF) groups associated with five MDM clusters. (C) Heatmap showing the scores of the MES-signatures among MDM clusters and other myeloid clusters. (D) Distribution of monocytes and MDM clusters along the pseudotime trajectory using Monocle2 (up); Ratio of MDMC2 cells in stage 1, stage 2 and stage 3-4-5 of pseudotime trajectory (down). (E) Density plots of switching genes for significantly over-represented functional ontologies. (F) T-SNE plots showing different identified types of MDM. (G) Intersection of switchgenes in our data and up-regulated genes in published data. (H) Feature plots and violin plots showing the expression of <t>TREM1</t> and SLC2A3 in MDM clusters and determining that MDMC2 specifically overexpressed TREM1. (I) Scatterplots showing significant correlations between TREM1 expression and the scoring of MES-myeloid signature in the MDMs of each sample. (J) Representative images of Multiplexed immunostaining of LGG, nGBM, and rGBM patients (n = 3). (K) Intersection signature genes of MES-MDM, MP-MES and MES-myeloid. (L) Representative FCM plots and summary data showing the percentage of TREM1 hi MDM in GBM tissues (n = 9). (M) Expression of the MES signature genes in TREM1 hi MDM and TREM1 lo MDM in primary cells.
    Pe Cy7 Anti Mouse Trem1, supplied by Bioss, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    R&D Systems anti trem1
    scRNA-seq reveals a new MES-MDM in patients with GBM. (A) T-SNE plots showing unsupervised clusters of nine cell types superclusters. The nine superclusters are: cancer cell, monocyte-derived macrophages (MDM), monocyte, microglial Cells (MGcells), endothelial cells (ECs), lymphocytes, oligodendrocyte, stromal cells (SCs), and neutrophils. Dots represent individual cells, and colors represent different cell populations. (B) The SCENIC analysis identified five transcription factor (TF) groups associated with five MDM clusters. (C) Heatmap showing the scores of the MES-signatures among MDM clusters and other myeloid clusters. (D) Distribution of monocytes and MDM clusters along the pseudotime trajectory using Monocle2 (up); Ratio of MDMC2 cells in stage 1, stage 2 and stage 3-4-5 of pseudotime trajectory (down). (E) Density plots of switching genes for significantly over-represented functional ontologies. (F) T-SNE plots showing different identified types of MDM. (G) Intersection of switchgenes in our data and up-regulated genes in published data. (H) Feature plots and violin plots showing the expression of <t>TREM1</t> and SLC2A3 in MDM clusters and determining that MDMC2 specifically overexpressed TREM1. (I) Scatterplots showing significant correlations between TREM1 expression and the scoring of MES-myeloid signature in the MDMs of each sample. (J) Representative images of Multiplexed immunostaining of LGG, nGBM, and rGBM patients (n = 3). (K) Intersection signature genes of MES-MDM, MP-MES and MES-myeloid. (L) Representative FCM plots and summary data showing the percentage of TREM1 hi MDM in GBM tissues (n = 9). (M) Expression of the MES signature genes in TREM1 hi MDM and TREM1 lo MDM in primary cells.
    Anti Trem1, supplied by R&D Systems, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/anti+trem1/pm41782012-77-25-26?v=R%26D+Systems
    Average 94 stars, based on 1 article reviews
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    Bioss rabbit anti trem1 antibody
    A Venn diagram showing the overlap of upregulated differential genes in the <t>TREM1</t> + PMN-MDSCs subset and genes reported in the literature for PMN-MDSCs. B Bar plot displaying the enriched pathways for the intersecting genes. C Density plot showing the expression of the intersecting genes. D Heatmap showing the expression of immunosuppressive genes in neutrophil subsets. E Density plot showing the expression of the TREM1 gene. F The ridge plot displaying the expression of TREM1 in the PMN-MDSCs subgroup across various cancer types that contained ≥ 10 cells in this subgroup. G Proportional plot showing the distribution of neutrophil subsets across different cancer types. H Survival analysis displaying the prognosis of TREM1 + PMN-MDSCs. I Survival analysis displaying the prognosis of the TREM1 gene. J Multiplex immunofluorescence staining for TREM1 + PMN-MDSCs. DAPI (blue), ITGAM (red), OLR1 (green) and TREM1 (magenta) are shown in individual and merged channels. The yellow arrows point to cells positive for the three markers (LUSC, lung squamous cell carcinoma; KIRC, kidney renal clear cell carcinoma). K Compared with the T cell group, the function of T cells was inhibited after co-culture with MDSCs. When MDSCs co-cultured with tumor cells were added to T cells, the inhibition of T cell function became more significant. The statistical method used was an unpaired t -test. Error bars represent the standard error (SE). * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.
    Rabbit Anti Trem1 Antibody, supplied by Bioss, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/anti+trem1/pmc12820143-345-23-27?v=Bioss
    Average 94 stars, based on 1 article reviews
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    trem1  (Bioss)
    94
    Bioss trem1
    Expression of <t>CD46/TREM1</t> and LC3B/ATG5 in four stages of SD rats: normal (NC), inflammatory (INF), leukoplakia (OLK), and squamous cell carcinoma (OSCC) (×20).
    Trem1, supplied by Bioss, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    93
    Proteintech trem1
    a Top left, UMAP plot of 9542 cell colors by myeloid cell types. Gray circle: Mφ. Bottom left, UMAP plot displayed the differential abundance (DA) myeloid cells of the inflammatory development of oral mucosal epithelium. Red: DA myeloid cells in REOLP. Blue: DA myeloid cells in NREOLP. Gray circle: DA Mφ in REOLP. Top right, UMAP plot of 6,680 cell colors by Mφ types. Gray circle: DA Mφ in REOLP. Bottom right, violin plot of the expression of IL1B in different Mφ subtypes. b Scatterplot and network plot showing the active transcription factors of <t>TREM1</t> + Mφ and the PPI of active transcription factors and IL-1β. c Ridge plots showed the differential expression of signaling pathways in TREM1 + Mφ and TREM1 - Mφ. d Circle plot of the intercellular communication (IC) from pyroptotic epithelial cells (top) and TREM1 + Mφ (bottom) to other cells in the inflammatory development of oral mucosal epithelium. Line width, the IC strength. Red arrow, the IC strength in REOLP was higher than in NREOLP. Blue arrow, the IC strength in NREOLP was higher than in REOLP. e Top left, UMAP plot of 75,336 cells colors by NK/T cell types. Gray circle: Th17 cells. Bottom left, UMAP plot displayed the DA NK/T cells of the inflammatory development of oral mucosal epithelium. Red: DA NK/T cells in REOLP. Blue: DA NK/T cells in NREOLP. Gray circle: DA Th17 cells in REOLP. Right, UMAP plot of 10,954 cell colors by Th17 cell types. Gray circle: DA Th17 cells in REOLP. f Left, dot plot of the IC from TREM1 + Mφ to naïve CD4 + T cells in IL1 signaling pathway in the inflammatory development of oral mucosal epithelium. Dot size, p-value; color scale, IC probability. Right, the developmental trajectory of T cell subtypes. g Bar plot exhibiting the upregulated signaling pathways of pathogenic Th17 cells in the inflammatory development of oral mucosal epithelium.
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    Proteintech il 17a
    a Flow chart of cytological experiments. b Flow cytometry showing the TREM1 expression of the TREM1 + Mφ and TREM1 NC Mφ. c Elisa assay depicting the concentration of IL-1β in TREM1 + Mφ and TREM1 NC Mφ with/without the stimulation of recombinant human HMGB1 (rhHMGB1), respectively. Note: ** p < 0.01, NS not statistically significant. Flow cytometry ( d ) and statistical analysis ( e ) of the c e ll proportion of CD4 + <t>IL-17A</t> + cells, CD4 + IL-17F + cells, and CD4 + IL-22 + cells after murine naïve CD4 + T cells co - cultured with the supernatants of TREM1 + Mφ, IL-6 and IL-23, with/without neutralizing anti-IL-1β (α-IL-1β). Note: * p < 0.05, ** p < 0.01, NS not statistically significant. f Representative images of mIHC in NREOLP (top) and REOLP (bottom). Scale bars: 100 µM (top) and 50 µM (bottom). Yellow arrows pointed to LPS + GSDMD + E-cad + cells. Red arrows pointed to TREM1 + CD68 + cells. Green arrows pointed to IL-17A + CD3 + cells.
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    Image Search Results


    scRNA-seq reveals a new MES-MDM in patients with GBM. (A) T-SNE plots showing unsupervised clusters of nine cell types superclusters. The nine superclusters are: cancer cell, monocyte-derived macrophages (MDM), monocyte, microglial Cells (MGcells), endothelial cells (ECs), lymphocytes, oligodendrocyte, stromal cells (SCs), and neutrophils. Dots represent individual cells, and colors represent different cell populations. (B) The SCENIC analysis identified five transcription factor (TF) groups associated with five MDM clusters. (C) Heatmap showing the scores of the MES-signatures among MDM clusters and other myeloid clusters. (D) Distribution of monocytes and MDM clusters along the pseudotime trajectory using Monocle2 (up); Ratio of MDMC2 cells in stage 1, stage 2 and stage 3-4-5 of pseudotime trajectory (down). (E) Density plots of switching genes for significantly over-represented functional ontologies. (F) T-SNE plots showing different identified types of MDM. (G) Intersection of switchgenes in our data and up-regulated genes in published data. (H) Feature plots and violin plots showing the expression of TREM1 and SLC2A3 in MDM clusters and determining that MDMC2 specifically overexpressed TREM1. (I) Scatterplots showing significant correlations between TREM1 expression and the scoring of MES-myeloid signature in the MDMs of each sample. (J) Representative images of Multiplexed immunostaining of LGG, nGBM, and rGBM patients (n = 3). (K) Intersection signature genes of MES-MDM, MP-MES and MES-myeloid. (L) Representative FCM plots and summary data showing the percentage of TREM1 hi MDM in GBM tissues (n = 9). (M) Expression of the MES signature genes in TREM1 hi MDM and TREM1 lo MDM in primary cells.

    Journal: Journal of Advanced Research

    Article Title: Targeting mesenchymal monocyte-derived macrophages to enhance the sensitivity of glioblastoma to temozolomide by inhibiting TNF/CELSR2/p65/Kla-HDAC1/EPAS1 axis

    doi: 10.1016/j.jare.2025.05.032

    Figure Lengend Snippet: scRNA-seq reveals a new MES-MDM in patients with GBM. (A) T-SNE plots showing unsupervised clusters of nine cell types superclusters. The nine superclusters are: cancer cell, monocyte-derived macrophages (MDM), monocyte, microglial Cells (MGcells), endothelial cells (ECs), lymphocytes, oligodendrocyte, stromal cells (SCs), and neutrophils. Dots represent individual cells, and colors represent different cell populations. (B) The SCENIC analysis identified five transcription factor (TF) groups associated with five MDM clusters. (C) Heatmap showing the scores of the MES-signatures among MDM clusters and other myeloid clusters. (D) Distribution of monocytes and MDM clusters along the pseudotime trajectory using Monocle2 (up); Ratio of MDMC2 cells in stage 1, stage 2 and stage 3-4-5 of pseudotime trajectory (down). (E) Density plots of switching genes for significantly over-represented functional ontologies. (F) T-SNE plots showing different identified types of MDM. (G) Intersection of switchgenes in our data and up-regulated genes in published data. (H) Feature plots and violin plots showing the expression of TREM1 and SLC2A3 in MDM clusters and determining that MDMC2 specifically overexpressed TREM1. (I) Scatterplots showing significant correlations between TREM1 expression and the scoring of MES-myeloid signature in the MDMs of each sample. (J) Representative images of Multiplexed immunostaining of LGG, nGBM, and rGBM patients (n = 3). (K) Intersection signature genes of MES-MDM, MP-MES and MES-myeloid. (L) Representative FCM plots and summary data showing the percentage of TREM1 hi MDM in GBM tissues (n = 9). (M) Expression of the MES signature genes in TREM1 hi MDM and TREM1 lo MDM in primary cells.

    Article Snippet: The antibodies used included anti-human CD68 (abcam, ab955), anti-human TMEM119 (abcam, ab306583), anti-human TREM1 (abcam, ab225861), anti-human GLUT1 (abcam, ab115730), anti-human CD44 (abcam, ab254530), anti-human CD24, anti-human EGFR (abcam, ab52894), anti-human HIF1α (abcam, ab51608), anti-human p65 (abcam, ab32536), anti-human ATF3 (abcam, ab254268), anti-human FOSL2 (proteintech, 15832-1-AP), anti-human GAPDH (proteintech, 10494-1-AP), anti-human EPAS1 (proteintech, 83790-1-RR), anti-human CEBPD (huabio, ER62841), anti-human TNF (abcam, ab183218), anti-human CELSR2 (Biomatik, CAU22255), anti-human Pan-Lactyl-lysine (huabio, PSH03-74), anti-human HDAC1 (huabio, SY12-04), anti-mouse CD4 (huabio, ET1609-52), anti-mouse Il7r (huabio, HA721214), anti-mouse PD-1 (abcam, ab214421), anti-mouse CD16/32 (BioLegend, #101302), APC/cy7 anti-mouse CD45 (BioLegend, #103115), PE/Dazzle 594 anti-mouse CD3 (BioLegend, #100245), PerCP/cy5.5 anti-mouse CD4 (BioLegend, #100434), AF647 anti-mouse FOXP3 (BioLegend, #126407), PE anti-mouse PD-1 (BioLegend, #135205), Brilliant Violet 711 anti- mouse CD11b (BioLegend, #101242), AF488 anti-mouse IL7R (BioLegend, #135017), FITC anti-mouse Ly-6G (BioLegend, #127605), PB anti-mouse Ly-6C (BioLegend, #128013), BV421 anti-mouse PD-1 (BD Biosciences, #562584), FITC anti-mouse IL7R (BioLegend, #135007), PE anti-mouse F4/80 (BioLegend, #123109), PE-cy7 anti-mouse TREM1 (Bioss, bs-4886R), AF488 anti-mouse P2Y12 (Bioss, 12072R), anti-human FcX (BioLegend, #163403), PB anti-human CD44 (BioLegend, #338823), PE-cy7 anti-human CD24 (BD Biosciences, #561646), PE anti-human PDGFRA (ebioscience, #12140181), AF488 anti-human EGFR (BioLegend, #352907), APC/cy7 anti-human CD45 (BioLegend, #368516), FITC anti-human CD3 (BioLegend, #981002), PerCP/cy5.5 anti-human CD4 (BioLegend, #300529), APC anti-human Foxp3 (ebioscience, #17477642), APC anti-human IL7R (ebioscience, #17127842), PE anti-human PD-1 (Bioss, bc12075463), AF647 anti-human CD68 (BioLegend, #333820), AF488 anti-human P2Y12 (Bioss, bc08034611), PE anti-human TREM1 (BioLegend, #314906).

    Techniques: Derivative Assay, Functional Assay, Expressing, Immunostaining

    Pro-tumor function of MES-MDM. (A) Heatmap showing the proportions of MDM clusters in GBM using TCGA-GBM/LGG cohort (n = 493). LGG: low grade gliomas. MGMT: O6-methylguanine-DNA methyltransferase. EGFR: epidermal growth factor receptor. TERT: telomerase reverse transcriptase. Chr: chromosome. Co: co-deletion. CL: classical. PN: proneural. NE: neural. MES: mesenchymal. BRAF V600E: BRAF proto-oncogene, serine/threonine kinase V600E mutation. NA: not applicable. G2: Grade 2. G3: Grade 3. G4: Grade 4. (B) and (C) Boxplots display the estimated proportions of MDM clusters in different histology (B) or subtypes (C) using TCGA-GBM/LGG cohort (n = 493) CL: classical. PN: proneural. NE: neural. MES: mesenchymal. G2: Grade 2. G3: Grade 3. G4: Grade 4. Center line shows median, box limits indicate the upper and lower quartiles, and whiskers extend 1.5 times the interquartile range. *, p < 0.05. ns, not significant. A two-sided unpaired Wilcoxon test was conducted. (D) The overall survival of patients in the CGGA-GBM/LGG cohort (n = 229) was analyzed using multivariate Cox regression. Forest plots with error bars display the confidence interval, indicating the lower bound at 2.5 % and the higher bound at 97.5 %. (E) Feature plots and violin plots showing the scoring of the MES-MDM signature in LGG, nGBM, and rGBM using GSE182109 data. (F) Schematic illustration of mPBMC-derived MDM treatment schedule in an orthotopic GBM model. (G) Bioluminescence analysis of orthotopic tumor growth over time, n = 5. (H) Survival curve of GBM-bearing mice with mPBMC-derived TREM1 hi MDM or TREM1 lo MDM treatment (n = 5 mice). (I) Bioluminescence images in tumor-bearing mice treated with mPBMC-derived MDM were quantified at day 20, 30, and 40.

    Journal: Journal of Advanced Research

    Article Title: Targeting mesenchymal monocyte-derived macrophages to enhance the sensitivity of glioblastoma to temozolomide by inhibiting TNF/CELSR2/p65/Kla-HDAC1/EPAS1 axis

    doi: 10.1016/j.jare.2025.05.032

    Figure Lengend Snippet: Pro-tumor function of MES-MDM. (A) Heatmap showing the proportions of MDM clusters in GBM using TCGA-GBM/LGG cohort (n = 493). LGG: low grade gliomas. MGMT: O6-methylguanine-DNA methyltransferase. EGFR: epidermal growth factor receptor. TERT: telomerase reverse transcriptase. Chr: chromosome. Co: co-deletion. CL: classical. PN: proneural. NE: neural. MES: mesenchymal. BRAF V600E: BRAF proto-oncogene, serine/threonine kinase V600E mutation. NA: not applicable. G2: Grade 2. G3: Grade 3. G4: Grade 4. (B) and (C) Boxplots display the estimated proportions of MDM clusters in different histology (B) or subtypes (C) using TCGA-GBM/LGG cohort (n = 493) CL: classical. PN: proneural. NE: neural. MES: mesenchymal. G2: Grade 2. G3: Grade 3. G4: Grade 4. Center line shows median, box limits indicate the upper and lower quartiles, and whiskers extend 1.5 times the interquartile range. *, p < 0.05. ns, not significant. A two-sided unpaired Wilcoxon test was conducted. (D) The overall survival of patients in the CGGA-GBM/LGG cohort (n = 229) was analyzed using multivariate Cox regression. Forest plots with error bars display the confidence interval, indicating the lower bound at 2.5 % and the higher bound at 97.5 %. (E) Feature plots and violin plots showing the scoring of the MES-MDM signature in LGG, nGBM, and rGBM using GSE182109 data. (F) Schematic illustration of mPBMC-derived MDM treatment schedule in an orthotopic GBM model. (G) Bioluminescence analysis of orthotopic tumor growth over time, n = 5. (H) Survival curve of GBM-bearing mice with mPBMC-derived TREM1 hi MDM or TREM1 lo MDM treatment (n = 5 mice). (I) Bioluminescence images in tumor-bearing mice treated with mPBMC-derived MDM were quantified at day 20, 30, and 40.

    Article Snippet: The antibodies used included anti-human CD68 (abcam, ab955), anti-human TMEM119 (abcam, ab306583), anti-human TREM1 (abcam, ab225861), anti-human GLUT1 (abcam, ab115730), anti-human CD44 (abcam, ab254530), anti-human CD24, anti-human EGFR (abcam, ab52894), anti-human HIF1α (abcam, ab51608), anti-human p65 (abcam, ab32536), anti-human ATF3 (abcam, ab254268), anti-human FOSL2 (proteintech, 15832-1-AP), anti-human GAPDH (proteintech, 10494-1-AP), anti-human EPAS1 (proteintech, 83790-1-RR), anti-human CEBPD (huabio, ER62841), anti-human TNF (abcam, ab183218), anti-human CELSR2 (Biomatik, CAU22255), anti-human Pan-Lactyl-lysine (huabio, PSH03-74), anti-human HDAC1 (huabio, SY12-04), anti-mouse CD4 (huabio, ET1609-52), anti-mouse Il7r (huabio, HA721214), anti-mouse PD-1 (abcam, ab214421), anti-mouse CD16/32 (BioLegend, #101302), APC/cy7 anti-mouse CD45 (BioLegend, #103115), PE/Dazzle 594 anti-mouse CD3 (BioLegend, #100245), PerCP/cy5.5 anti-mouse CD4 (BioLegend, #100434), AF647 anti-mouse FOXP3 (BioLegend, #126407), PE anti-mouse PD-1 (BioLegend, #135205), Brilliant Violet 711 anti- mouse CD11b (BioLegend, #101242), AF488 anti-mouse IL7R (BioLegend, #135017), FITC anti-mouse Ly-6G (BioLegend, #127605), PB anti-mouse Ly-6C (BioLegend, #128013), BV421 anti-mouse PD-1 (BD Biosciences, #562584), FITC anti-mouse IL7R (BioLegend, #135007), PE anti-mouse F4/80 (BioLegend, #123109), PE-cy7 anti-mouse TREM1 (Bioss, bs-4886R), AF488 anti-mouse P2Y12 (Bioss, 12072R), anti-human FcX (BioLegend, #163403), PB anti-human CD44 (BioLegend, #338823), PE-cy7 anti-human CD24 (BD Biosciences, #561646), PE anti-human PDGFRA (ebioscience, #12140181), AF488 anti-human EGFR (BioLegend, #352907), APC/cy7 anti-human CD45 (BioLegend, #368516), FITC anti-human CD3 (BioLegend, #981002), PerCP/cy5.5 anti-human CD4 (BioLegend, #300529), APC anti-human Foxp3 (ebioscience, #17477642), APC anti-human IL7R (ebioscience, #17127842), PE anti-human PD-1 (Bioss, bc12075463), AF647 anti-human CD68 (BioLegend, #333820), AF488 anti-human P2Y12 (Bioss, bc08034611), PE anti-human TREM1 (BioLegend, #314906).

    Techniques: Reverse Transcription, Mutagenesis, Derivative Assay

    Hypoxia induces the MES-MDM signature. (A) Boxplots displaying estimated proportions of MDM clusters in different spatial position of hGBMs using bulk RNA-seq data from the Ivy-hGBM cohort (n = 270). ∗, p < 0.05. (B) Surface plots showing the transcriptional programs of MDM clusters at the spatial level using published hGBM spatial transcriptomics data. (C) Immunostaining of CD68, TMEM119, TREM1, and GLUT1 in the peri-necrotic region of hGBM. Scale bar = 100 μm. (D) Visualization of distinct switching genes from the two paths filtered by the McFadden’s Pseudo R2. (E) Intersection of TFs of switch genes in branch1 and branch2, and the correlations between intersection TFs and TREM1 expression in CGGA-GBM cohort (n = 386). (F) Representative images of western blotting of p65 in hPBMC-derived MDM with the indicated treatment. (G) Relevant images depicting the western blot analysis of HIF-1a, p65, ATF3, FOSL2, TREM1 in hPBMC-derived MDM treated as indicated are presented. (H) STRING analysis revealed the interaction between p65, ATF3, and FOSL2. (I) Relative expression of MES-MDM signature genes after knockdown of ATF3 and FOSL2 in hPBMC-derived MDM.

    Journal: Journal of Advanced Research

    Article Title: Targeting mesenchymal monocyte-derived macrophages to enhance the sensitivity of glioblastoma to temozolomide by inhibiting TNF/CELSR2/p65/Kla-HDAC1/EPAS1 axis

    doi: 10.1016/j.jare.2025.05.032

    Figure Lengend Snippet: Hypoxia induces the MES-MDM signature. (A) Boxplots displaying estimated proportions of MDM clusters in different spatial position of hGBMs using bulk RNA-seq data from the Ivy-hGBM cohort (n = 270). ∗, p < 0.05. (B) Surface plots showing the transcriptional programs of MDM clusters at the spatial level using published hGBM spatial transcriptomics data. (C) Immunostaining of CD68, TMEM119, TREM1, and GLUT1 in the peri-necrotic region of hGBM. Scale bar = 100 μm. (D) Visualization of distinct switching genes from the two paths filtered by the McFadden’s Pseudo R2. (E) Intersection of TFs of switch genes in branch1 and branch2, and the correlations between intersection TFs and TREM1 expression in CGGA-GBM cohort (n = 386). (F) Representative images of western blotting of p65 in hPBMC-derived MDM with the indicated treatment. (G) Relevant images depicting the western blot analysis of HIF-1a, p65, ATF3, FOSL2, TREM1 in hPBMC-derived MDM treated as indicated are presented. (H) STRING analysis revealed the interaction between p65, ATF3, and FOSL2. (I) Relative expression of MES-MDM signature genes after knockdown of ATF3 and FOSL2 in hPBMC-derived MDM.

    Article Snippet: The antibodies used included anti-human CD68 (abcam, ab955), anti-human TMEM119 (abcam, ab306583), anti-human TREM1 (abcam, ab225861), anti-human GLUT1 (abcam, ab115730), anti-human CD44 (abcam, ab254530), anti-human CD24, anti-human EGFR (abcam, ab52894), anti-human HIF1α (abcam, ab51608), anti-human p65 (abcam, ab32536), anti-human ATF3 (abcam, ab254268), anti-human FOSL2 (proteintech, 15832-1-AP), anti-human GAPDH (proteintech, 10494-1-AP), anti-human EPAS1 (proteintech, 83790-1-RR), anti-human CEBPD (huabio, ER62841), anti-human TNF (abcam, ab183218), anti-human CELSR2 (Biomatik, CAU22255), anti-human Pan-Lactyl-lysine (huabio, PSH03-74), anti-human HDAC1 (huabio, SY12-04), anti-mouse CD4 (huabio, ET1609-52), anti-mouse Il7r (huabio, HA721214), anti-mouse PD-1 (abcam, ab214421), anti-mouse CD16/32 (BioLegend, #101302), APC/cy7 anti-mouse CD45 (BioLegend, #103115), PE/Dazzle 594 anti-mouse CD3 (BioLegend, #100245), PerCP/cy5.5 anti-mouse CD4 (BioLegend, #100434), AF647 anti-mouse FOXP3 (BioLegend, #126407), PE anti-mouse PD-1 (BioLegend, #135205), Brilliant Violet 711 anti- mouse CD11b (BioLegend, #101242), AF488 anti-mouse IL7R (BioLegend, #135017), FITC anti-mouse Ly-6G (BioLegend, #127605), PB anti-mouse Ly-6C (BioLegend, #128013), BV421 anti-mouse PD-1 (BD Biosciences, #562584), FITC anti-mouse IL7R (BioLegend, #135007), PE anti-mouse F4/80 (BioLegend, #123109), PE-cy7 anti-mouse TREM1 (Bioss, bs-4886R), AF488 anti-mouse P2Y12 (Bioss, 12072R), anti-human FcX (BioLegend, #163403), PB anti-human CD44 (BioLegend, #338823), PE-cy7 anti-human CD24 (BD Biosciences, #561646), PE anti-human PDGFRA (ebioscience, #12140181), AF488 anti-human EGFR (BioLegend, #352907), APC/cy7 anti-human CD45 (BioLegend, #368516), FITC anti-human CD3 (BioLegend, #981002), PerCP/cy5.5 anti-human CD4 (BioLegend, #300529), APC anti-human Foxp3 (ebioscience, #17477642), APC anti-human IL7R (ebioscience, #17127842), PE anti-human PD-1 (Bioss, bc12075463), AF647 anti-human CD68 (BioLegend, #333820), AF488 anti-human P2Y12 (Bioss, bc08034611), PE anti-human TREM1 (BioLegend, #314906).

    Techniques: RNA Sequencing, Immunostaining, Expressing, Western Blot, Derivative Assay, Knockdown

    MES-MDM promote MES subtype transition of cancer cells. (A) T-SNE plots and percentage of cell types showing the single-cell landscape of samples with and without MES-MDM enrichment. The pie chart presents the proportion of cancer cells of the four subtypes among all cancer cells in the two groups: Enrichment group (G3, G4, G14, G18, G19, G22 sample), non-enrichment group (G15, G17, G21 sample). (B) Relative expression of MES-cancer cells signature genes after co-culturing with primary-TREM1 hi MDM or primary-TREM1 lo MDM. (C) A schematic diagram of the sorting and identification of NPC/OPC/MES/AC cancer cells from GBO. (D) Immunostaining for subtype-specific markers was performed on NPC/OPC/MES/AC cancer cells cultured by special culture medium. (E) Relative expression of signature genes in the cultured NPC/OPC/MES/AC-cancer cells. (F) Proportion of MES-cancer cells after co-culture of NPC-cancer cells and primary-MDM by FCM detection. (G) Inferred interaction ligand receptor pair between MES-MDM and cancer cells was analyzed using our hGBM scRNA-seq data by CellphoneDB analysis. (H) Representative images of western blotting of CD44 in GBO with the indicated treatment. (I) Representative images depicting the western blot analysis of CD44, p65, EPAS1, CEBPD, HDAC1 in prim-NPC-cancer cells treated as indicated. (J) Representative images depicting the western blot analysis of Pan-Kla in the proteins after IP by anti-HDAC1 antibody with the indicated treatment. (K) Representative images depicting the western blot analysis of Pan-Kla in the proteins after IP by anti-HDAC1 antibody with the indicated treatment, mut1 (K200: AAG-CGA), mut2 (K200: AAG-GCG). (L) Relative expression of MES-cancer cells signature genes with the indicated treatment in NPC-cancer cells.

    Journal: Journal of Advanced Research

    Article Title: Targeting mesenchymal monocyte-derived macrophages to enhance the sensitivity of glioblastoma to temozolomide by inhibiting TNF/CELSR2/p65/Kla-HDAC1/EPAS1 axis

    doi: 10.1016/j.jare.2025.05.032

    Figure Lengend Snippet: MES-MDM promote MES subtype transition of cancer cells. (A) T-SNE plots and percentage of cell types showing the single-cell landscape of samples with and without MES-MDM enrichment. The pie chart presents the proportion of cancer cells of the four subtypes among all cancer cells in the two groups: Enrichment group (G3, G4, G14, G18, G19, G22 sample), non-enrichment group (G15, G17, G21 sample). (B) Relative expression of MES-cancer cells signature genes after co-culturing with primary-TREM1 hi MDM or primary-TREM1 lo MDM. (C) A schematic diagram of the sorting and identification of NPC/OPC/MES/AC cancer cells from GBO. (D) Immunostaining for subtype-specific markers was performed on NPC/OPC/MES/AC cancer cells cultured by special culture medium. (E) Relative expression of signature genes in the cultured NPC/OPC/MES/AC-cancer cells. (F) Proportion of MES-cancer cells after co-culture of NPC-cancer cells and primary-MDM by FCM detection. (G) Inferred interaction ligand receptor pair between MES-MDM and cancer cells was analyzed using our hGBM scRNA-seq data by CellphoneDB analysis. (H) Representative images of western blotting of CD44 in GBO with the indicated treatment. (I) Representative images depicting the western blot analysis of CD44, p65, EPAS1, CEBPD, HDAC1 in prim-NPC-cancer cells treated as indicated. (J) Representative images depicting the western blot analysis of Pan-Kla in the proteins after IP by anti-HDAC1 antibody with the indicated treatment. (K) Representative images depicting the western blot analysis of Pan-Kla in the proteins after IP by anti-HDAC1 antibody with the indicated treatment, mut1 (K200: AAG-CGA), mut2 (K200: AAG-GCG). (L) Relative expression of MES-cancer cells signature genes with the indicated treatment in NPC-cancer cells.

    Article Snippet: The antibodies used included anti-human CD68 (abcam, ab955), anti-human TMEM119 (abcam, ab306583), anti-human TREM1 (abcam, ab225861), anti-human GLUT1 (abcam, ab115730), anti-human CD44 (abcam, ab254530), anti-human CD24, anti-human EGFR (abcam, ab52894), anti-human HIF1α (abcam, ab51608), anti-human p65 (abcam, ab32536), anti-human ATF3 (abcam, ab254268), anti-human FOSL2 (proteintech, 15832-1-AP), anti-human GAPDH (proteintech, 10494-1-AP), anti-human EPAS1 (proteintech, 83790-1-RR), anti-human CEBPD (huabio, ER62841), anti-human TNF (abcam, ab183218), anti-human CELSR2 (Biomatik, CAU22255), anti-human Pan-Lactyl-lysine (huabio, PSH03-74), anti-human HDAC1 (huabio, SY12-04), anti-mouse CD4 (huabio, ET1609-52), anti-mouse Il7r (huabio, HA721214), anti-mouse PD-1 (abcam, ab214421), anti-mouse CD16/32 (BioLegend, #101302), APC/cy7 anti-mouse CD45 (BioLegend, #103115), PE/Dazzle 594 anti-mouse CD3 (BioLegend, #100245), PerCP/cy5.5 anti-mouse CD4 (BioLegend, #100434), AF647 anti-mouse FOXP3 (BioLegend, #126407), PE anti-mouse PD-1 (BioLegend, #135205), Brilliant Violet 711 anti- mouse CD11b (BioLegend, #101242), AF488 anti-mouse IL7R (BioLegend, #135017), FITC anti-mouse Ly-6G (BioLegend, #127605), PB anti-mouse Ly-6C (BioLegend, #128013), BV421 anti-mouse PD-1 (BD Biosciences, #562584), FITC anti-mouse IL7R (BioLegend, #135007), PE anti-mouse F4/80 (BioLegend, #123109), PE-cy7 anti-mouse TREM1 (Bioss, bs-4886R), AF488 anti-mouse P2Y12 (Bioss, 12072R), anti-human FcX (BioLegend, #163403), PB anti-human CD44 (BioLegend, #338823), PE-cy7 anti-human CD24 (BD Biosciences, #561646), PE anti-human PDGFRA (ebioscience, #12140181), AF488 anti-human EGFR (BioLegend, #352907), APC/cy7 anti-human CD45 (BioLegend, #368516), FITC anti-human CD3 (BioLegend, #981002), PerCP/cy5.5 anti-human CD4 (BioLegend, #300529), APC anti-human Foxp3 (ebioscience, #17477642), APC anti-human IL7R (ebioscience, #17127842), PE anti-human PD-1 (Bioss, bc12075463), AF647 anti-human CD68 (BioLegend, #333820), AF488 anti-human P2Y12 (Bioss, bc08034611), PE anti-human TREM1 (BioLegend, #314906).

    Techniques: Expressing, Immunostaining, Cell Culture, Co-Culture Assay, Western Blot

    Targeting TREM1 enhances the efficacy of anti-PD-1 immunotherapy. (A) Relative expression of MES-cancer cells signature genes after TREM1 inhibitor treatment. (B) Relative expression of MES-cancer cells signature genes in the co-culture system. (C) and (D) Representative immunostaining images and quantitative analysis depicting CD44 in GBO which were co-cultured with hPBMC-derived MES-MDM. (E) Representative immunostaining images and quantitative analysis depicting KI67 in GBO which were co-cultured with hPBMC-derived MES-MDM with the treatment indicated. (F) Expression score of the IL7R + CD4 + T-cells signature genes of non-responder and responder after anti-PD-1 therapy. (G) Schematic illustration of anti-PD-1 and/or LP17 treatment in GBM-bearing mice. (H) Survival curve of GBM-bearing mice (n = 5 mice/group). (I) Percentage of Il7r + CD4 + T-cells in CD4 + T-cells of GBM-bearing mice with anti-PD-1 and/or LP17 treatment. (J) Percentage of exhaustion Il7r + CD4 + T-cells in Il7r + CD4 + T-cells of GBM-bearing mice with anti-PD-1 and/or LP17 treatment. (K) Representative images of multiplexed immunostaining from brains of GBM-bearing mice with anti-PD-1 and/or LP17 treatment. ∗∗, p < 0.01. ∗∗∗, p < 0.001.

    Journal: Journal of Advanced Research

    Article Title: Targeting mesenchymal monocyte-derived macrophages to enhance the sensitivity of glioblastoma to temozolomide by inhibiting TNF/CELSR2/p65/Kla-HDAC1/EPAS1 axis

    doi: 10.1016/j.jare.2025.05.032

    Figure Lengend Snippet: Targeting TREM1 enhances the efficacy of anti-PD-1 immunotherapy. (A) Relative expression of MES-cancer cells signature genes after TREM1 inhibitor treatment. (B) Relative expression of MES-cancer cells signature genes in the co-culture system. (C) and (D) Representative immunostaining images and quantitative analysis depicting CD44 in GBO which were co-cultured with hPBMC-derived MES-MDM. (E) Representative immunostaining images and quantitative analysis depicting KI67 in GBO which were co-cultured with hPBMC-derived MES-MDM with the treatment indicated. (F) Expression score of the IL7R + CD4 + T-cells signature genes of non-responder and responder after anti-PD-1 therapy. (G) Schematic illustration of anti-PD-1 and/or LP17 treatment in GBM-bearing mice. (H) Survival curve of GBM-bearing mice (n = 5 mice/group). (I) Percentage of Il7r + CD4 + T-cells in CD4 + T-cells of GBM-bearing mice with anti-PD-1 and/or LP17 treatment. (J) Percentage of exhaustion Il7r + CD4 + T-cells in Il7r + CD4 + T-cells of GBM-bearing mice with anti-PD-1 and/or LP17 treatment. (K) Representative images of multiplexed immunostaining from brains of GBM-bearing mice with anti-PD-1 and/or LP17 treatment. ∗∗, p < 0.01. ∗∗∗, p < 0.001.

    Article Snippet: The antibodies used included anti-human CD68 (abcam, ab955), anti-human TMEM119 (abcam, ab306583), anti-human TREM1 (abcam, ab225861), anti-human GLUT1 (abcam, ab115730), anti-human CD44 (abcam, ab254530), anti-human CD24, anti-human EGFR (abcam, ab52894), anti-human HIF1α (abcam, ab51608), anti-human p65 (abcam, ab32536), anti-human ATF3 (abcam, ab254268), anti-human FOSL2 (proteintech, 15832-1-AP), anti-human GAPDH (proteintech, 10494-1-AP), anti-human EPAS1 (proteintech, 83790-1-RR), anti-human CEBPD (huabio, ER62841), anti-human TNF (abcam, ab183218), anti-human CELSR2 (Biomatik, CAU22255), anti-human Pan-Lactyl-lysine (huabio, PSH03-74), anti-human HDAC1 (huabio, SY12-04), anti-mouse CD4 (huabio, ET1609-52), anti-mouse Il7r (huabio, HA721214), anti-mouse PD-1 (abcam, ab214421), anti-mouse CD16/32 (BioLegend, #101302), APC/cy7 anti-mouse CD45 (BioLegend, #103115), PE/Dazzle 594 anti-mouse CD3 (BioLegend, #100245), PerCP/cy5.5 anti-mouse CD4 (BioLegend, #100434), AF647 anti-mouse FOXP3 (BioLegend, #126407), PE anti-mouse PD-1 (BioLegend, #135205), Brilliant Violet 711 anti- mouse CD11b (BioLegend, #101242), AF488 anti-mouse IL7R (BioLegend, #135017), FITC anti-mouse Ly-6G (BioLegend, #127605), PB anti-mouse Ly-6C (BioLegend, #128013), BV421 anti-mouse PD-1 (BD Biosciences, #562584), FITC anti-mouse IL7R (BioLegend, #135007), PE anti-mouse F4/80 (BioLegend, #123109), PE-cy7 anti-mouse TREM1 (Bioss, bs-4886R), AF488 anti-mouse P2Y12 (Bioss, 12072R), anti-human FcX (BioLegend, #163403), PB anti-human CD44 (BioLegend, #338823), PE-cy7 anti-human CD24 (BD Biosciences, #561646), PE anti-human PDGFRA (ebioscience, #12140181), AF488 anti-human EGFR (BioLegend, #352907), APC/cy7 anti-human CD45 (BioLegend, #368516), FITC anti-human CD3 (BioLegend, #981002), PerCP/cy5.5 anti-human CD4 (BioLegend, #300529), APC anti-human Foxp3 (ebioscience, #17477642), APC anti-human IL7R (ebioscience, #17127842), PE anti-human PD-1 (Bioss, bc12075463), AF647 anti-human CD68 (BioLegend, #333820), AF488 anti-human P2Y12 (Bioss, bc08034611), PE anti-human TREM1 (BioLegend, #314906).

    Techniques: Expressing, Co-Culture Assay, Immunostaining, Cell Culture, Derivative Assay

    A Venn diagram showing the overlap of upregulated differential genes in the TREM1 + PMN-MDSCs subset and genes reported in the literature for PMN-MDSCs. B Bar plot displaying the enriched pathways for the intersecting genes. C Density plot showing the expression of the intersecting genes. D Heatmap showing the expression of immunosuppressive genes in neutrophil subsets. E Density plot showing the expression of the TREM1 gene. F The ridge plot displaying the expression of TREM1 in the PMN-MDSCs subgroup across various cancer types that contained ≥ 10 cells in this subgroup. G Proportional plot showing the distribution of neutrophil subsets across different cancer types. H Survival analysis displaying the prognosis of TREM1 + PMN-MDSCs. I Survival analysis displaying the prognosis of the TREM1 gene. J Multiplex immunofluorescence staining for TREM1 + PMN-MDSCs. DAPI (blue), ITGAM (red), OLR1 (green) and TREM1 (magenta) are shown in individual and merged channels. The yellow arrows point to cells positive for the three markers (LUSC, lung squamous cell carcinoma; KIRC, kidney renal clear cell carcinoma). K Compared with the T cell group, the function of T cells was inhibited after co-culture with MDSCs. When MDSCs co-cultured with tumor cells were added to T cells, the inhibition of T cell function became more significant. The statistical method used was an unpaired t -test. Error bars represent the standard error (SE). * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

    Journal: Communications Biology

    Article Title: Pan-cancer analysis reveals TREM1 + PMN-MDSCs as critical regulators of immune suppression and tumor microenvironment remodeling

    doi: 10.1038/s42003-025-09342-8

    Figure Lengend Snippet: A Venn diagram showing the overlap of upregulated differential genes in the TREM1 + PMN-MDSCs subset and genes reported in the literature for PMN-MDSCs. B Bar plot displaying the enriched pathways for the intersecting genes. C Density plot showing the expression of the intersecting genes. D Heatmap showing the expression of immunosuppressive genes in neutrophil subsets. E Density plot showing the expression of the TREM1 gene. F The ridge plot displaying the expression of TREM1 in the PMN-MDSCs subgroup across various cancer types that contained ≥ 10 cells in this subgroup. G Proportional plot showing the distribution of neutrophil subsets across different cancer types. H Survival analysis displaying the prognosis of TREM1 + PMN-MDSCs. I Survival analysis displaying the prognosis of the TREM1 gene. J Multiplex immunofluorescence staining for TREM1 + PMN-MDSCs. DAPI (blue), ITGAM (red), OLR1 (green) and TREM1 (magenta) are shown in individual and merged channels. The yellow arrows point to cells positive for the three markers (LUSC, lung squamous cell carcinoma; KIRC, kidney renal clear cell carcinoma). K Compared with the T cell group, the function of T cells was inhibited after co-culture with MDSCs. When MDSCs co-cultured with tumor cells were added to T cells, the inhibition of T cell function became more significant. The statistical method used was an unpaired t -test. Error bars represent the standard error (SE). * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

    Article Snippet: Primary antibodies employed in this study included: Anti- CD11b antibody (Abcam, ab52478, 1:400 dilution), Rabbit Anti- LOX1 antibody (Bioss, bs-2044R, 1:400 dilution) and Rabbit Anti- TREM1 antibody (Bioss, bs-10306R, 1:400 dilution).

    Techniques: Expressing, Multiplex Assay, Immunofluorescence, Staining, Co-Culture Assay, Cell Culture, Inhibition, Cell Function Assay

    A Scatter plot showing the correlation between TREM1 + PMN-MDSCs scores and gene sets across different cancer types. B Box plot displaying the scores of gene sets in high and low infiltration groups of TREM1 + PMN-MDSCs in bulk RNA-seq. C Scatter plot showing the correlation between TREM1 + PMN-MDSCs and other gene sets in bulk RNA-seq.

    Journal: Communications Biology

    Article Title: Pan-cancer analysis reveals TREM1 + PMN-MDSCs as critical regulators of immune suppression and tumor microenvironment remodeling

    doi: 10.1038/s42003-025-09342-8

    Figure Lengend Snippet: A Scatter plot showing the correlation between TREM1 + PMN-MDSCs scores and gene sets across different cancer types. B Box plot displaying the scores of gene sets in high and low infiltration groups of TREM1 + PMN-MDSCs in bulk RNA-seq. C Scatter plot showing the correlation between TREM1 + PMN-MDSCs and other gene sets in bulk RNA-seq.

    Article Snippet: Primary antibodies employed in this study included: Anti- CD11b antibody (Abcam, ab52478, 1:400 dilution), Rabbit Anti- LOX1 antibody (Bioss, bs-2044R, 1:400 dilution) and Rabbit Anti- TREM1 antibody (Bioss, bs-10306R, 1:400 dilution).

    Techniques: RNA Sequencing

    A Spatial feature plots of myeloid cells, TREM1 + PMN-MDSCs, fibroblasts, along with the immunosuppressive score, in tissue sections from breast cancer (BRCA), lung cancer (LC) and kidney clear cell carcinoma (KIRC). B Enhanced spatial feature plots showing the expression of OLR1 , TREM1 and COL1A1 in tumor tissues. C MistyR analysis showing the co-localization of TREM1 + PMN-MDSC with other cell types in KIRC. D Box plot showing the expression of exhausted T cells between high and low infiltration groups of TREM1 + PMN-MDSCs in KIRC. E Scatter plot showing the correlation between TREM1 + PMN-MDSCs and fibroblasts in KIRC. F Scatter plot showing the correlation between TREM1 + PMN-MDSCs and exhausted T cells in KIRC.

    Journal: Communications Biology

    Article Title: Pan-cancer analysis reveals TREM1 + PMN-MDSCs as critical regulators of immune suppression and tumor microenvironment remodeling

    doi: 10.1038/s42003-025-09342-8

    Figure Lengend Snippet: A Spatial feature plots of myeloid cells, TREM1 + PMN-MDSCs, fibroblasts, along with the immunosuppressive score, in tissue sections from breast cancer (BRCA), lung cancer (LC) and kidney clear cell carcinoma (KIRC). B Enhanced spatial feature plots showing the expression of OLR1 , TREM1 and COL1A1 in tumor tissues. C MistyR analysis showing the co-localization of TREM1 + PMN-MDSC with other cell types in KIRC. D Box plot showing the expression of exhausted T cells between high and low infiltration groups of TREM1 + PMN-MDSCs in KIRC. E Scatter plot showing the correlation between TREM1 + PMN-MDSCs and fibroblasts in KIRC. F Scatter plot showing the correlation between TREM1 + PMN-MDSCs and exhausted T cells in KIRC.

    Article Snippet: Primary antibodies employed in this study included: Anti- CD11b antibody (Abcam, ab52478, 1:400 dilution), Rabbit Anti- LOX1 antibody (Bioss, bs-2044R, 1:400 dilution) and Rabbit Anti- TREM1 antibody (Bioss, bs-10306R, 1:400 dilution).

    Techniques: Expressing

    A The cell‒cell interactions networks. B Scatter plots showing the strength of signal outgoing and incoming by different cell populations. C Chord plot showing the MHC-I and MIF signaling pathway networks. D Bubble plot showing ligand-receptor pairs of TREM1 + PMN-MDSCs as receivers interacting with other cell types. E Spatial feature plots showing the interaction activity of selected ligand-receptor pairs in KIRC tissue sections. F Top-ranked ligands inferred to regulate TREM1 + PMN-MDSC svia endothelial cells, fibroblasts, CD4 + Tregs, CD8 + Teffs and NK cells according to NicheNet. G Dot plot showing the expression percentage (dot size) and intensity (dot intensity) of top-ranked ligands in different cell types. H Heatmap depicting the regulatory relationships between ligands and target genes.

    Journal: Communications Biology

    Article Title: Pan-cancer analysis reveals TREM1 + PMN-MDSCs as critical regulators of immune suppression and tumor microenvironment remodeling

    doi: 10.1038/s42003-025-09342-8

    Figure Lengend Snippet: A The cell‒cell interactions networks. B Scatter plots showing the strength of signal outgoing and incoming by different cell populations. C Chord plot showing the MHC-I and MIF signaling pathway networks. D Bubble plot showing ligand-receptor pairs of TREM1 + PMN-MDSCs as receivers interacting with other cell types. E Spatial feature plots showing the interaction activity of selected ligand-receptor pairs in KIRC tissue sections. F Top-ranked ligands inferred to regulate TREM1 + PMN-MDSC svia endothelial cells, fibroblasts, CD4 + Tregs, CD8 + Teffs and NK cells according to NicheNet. G Dot plot showing the expression percentage (dot size) and intensity (dot intensity) of top-ranked ligands in different cell types. H Heatmap depicting the regulatory relationships between ligands and target genes.

    Article Snippet: Primary antibodies employed in this study included: Anti- CD11b antibody (Abcam, ab52478, 1:400 dilution), Rabbit Anti- LOX1 antibody (Bioss, bs-2044R, 1:400 dilution) and Rabbit Anti- TREM1 antibody (Bioss, bs-10306R, 1:400 dilution).

    Techniques: Activity Assay, Expressing

    Expression of CD46/TREM1 and LC3B/ATG5 in four stages of SD rats: normal (NC), inflammatory (INF), leukoplakia (OLK), and squamous cell carcinoma (OSCC) (×20).

    Journal: Frontiers in Molecular Biosciences

    Article Title: Exploring the interaction mechanisms of CD46/TREM1 and LC3B/ATG5 in the inflammation-cancer transformation of oral squamous cell carcinoma based on bioinformatics

    doi: 10.3389/fmolb.2025.1713632

    Figure Lengend Snippet: Expression of CD46/TREM1 and LC3B/ATG5 in four stages of SD rats: normal (NC), inflammatory (INF), leukoplakia (OLK), and squamous cell carcinoma (OSCC) (×20).

    Article Snippet: Primary antibodies used: CD46 (1:500, MCE, HY-P 80064), TREM1 (1:300, Bioss, bs-10306R), LC3B (1:100, MCE, HY-P 80742), ATG5 (1:600, Immunoway, YM8340).

    Techniques: Expressing

    Expression of CD46/TREM1 and LC3B/ATG5 in human normal (NC), leukoplakia (OLK), and squamous cell carcinoma (OSCC) tissues (×20).

    Journal: Frontiers in Molecular Biosciences

    Article Title: Exploring the interaction mechanisms of CD46/TREM1 and LC3B/ATG5 in the inflammation-cancer transformation of oral squamous cell carcinoma based on bioinformatics

    doi: 10.3389/fmolb.2025.1713632

    Figure Lengend Snippet: Expression of CD46/TREM1 and LC3B/ATG5 in human normal (NC), leukoplakia (OLK), and squamous cell carcinoma (OSCC) tissues (×20).

    Article Snippet: Primary antibodies used: CD46 (1:500, MCE, HY-P 80064), TREM1 (1:300, Bioss, bs-10306R), LC3B (1:100, MCE, HY-P 80742), ATG5 (1:600, Immunoway, YM8340).

    Techniques: Expressing

    a Top left, UMAP plot of 9542 cell colors by myeloid cell types. Gray circle: Mφ. Bottom left, UMAP plot displayed the differential abundance (DA) myeloid cells of the inflammatory development of oral mucosal epithelium. Red: DA myeloid cells in REOLP. Blue: DA myeloid cells in NREOLP. Gray circle: DA Mφ in REOLP. Top right, UMAP plot of 6,680 cell colors by Mφ types. Gray circle: DA Mφ in REOLP. Bottom right, violin plot of the expression of IL1B in different Mφ subtypes. b Scatterplot and network plot showing the active transcription factors of TREM1 + Mφ and the PPI of active transcription factors and IL-1β. c Ridge plots showed the differential expression of signaling pathways in TREM1 + Mφ and TREM1 - Mφ. d Circle plot of the intercellular communication (IC) from pyroptotic epithelial cells (top) and TREM1 + Mφ (bottom) to other cells in the inflammatory development of oral mucosal epithelium. Line width, the IC strength. Red arrow, the IC strength in REOLP was higher than in NREOLP. Blue arrow, the IC strength in NREOLP was higher than in REOLP. e Top left, UMAP plot of 75,336 cells colors by NK/T cell types. Gray circle: Th17 cells. Bottom left, UMAP plot displayed the DA NK/T cells of the inflammatory development of oral mucosal epithelium. Red: DA NK/T cells in REOLP. Blue: DA NK/T cells in NREOLP. Gray circle: DA Th17 cells in REOLP. Right, UMAP plot of 10,954 cell colors by Th17 cell types. Gray circle: DA Th17 cells in REOLP. f Left, dot plot of the IC from TREM1 + Mφ to naïve CD4 + T cells in IL1 signaling pathway in the inflammatory development of oral mucosal epithelium. Dot size, p-value; color scale, IC probability. Right, the developmental trajectory of T cell subtypes. g Bar plot exhibiting the upregulated signaling pathways of pathogenic Th17 cells in the inflammatory development of oral mucosal epithelium.

    Journal: Cell Death Discovery

    Article Title: Epithelial pyroptosis-induced TREM1 + macrophages activate Th17 cells to accelerate oral mucosal inflammation

    doi: 10.1038/s41420-025-02853-7

    Figure Lengend Snippet: a Top left, UMAP plot of 9542 cell colors by myeloid cell types. Gray circle: Mφ. Bottom left, UMAP plot displayed the differential abundance (DA) myeloid cells of the inflammatory development of oral mucosal epithelium. Red: DA myeloid cells in REOLP. Blue: DA myeloid cells in NREOLP. Gray circle: DA Mφ in REOLP. Top right, UMAP plot of 6,680 cell colors by Mφ types. Gray circle: DA Mφ in REOLP. Bottom right, violin plot of the expression of IL1B in different Mφ subtypes. b Scatterplot and network plot showing the active transcription factors of TREM1 + Mφ and the PPI of active transcription factors and IL-1β. c Ridge plots showed the differential expression of signaling pathways in TREM1 + Mφ and TREM1 - Mφ. d Circle plot of the intercellular communication (IC) from pyroptotic epithelial cells (top) and TREM1 + Mφ (bottom) to other cells in the inflammatory development of oral mucosal epithelium. Line width, the IC strength. Red arrow, the IC strength in REOLP was higher than in NREOLP. Blue arrow, the IC strength in NREOLP was higher than in REOLP. e Top left, UMAP plot of 75,336 cells colors by NK/T cell types. Gray circle: Th17 cells. Bottom left, UMAP plot displayed the DA NK/T cells of the inflammatory development of oral mucosal epithelium. Red: DA NK/T cells in REOLP. Blue: DA NK/T cells in NREOLP. Gray circle: DA Th17 cells in REOLP. Right, UMAP plot of 10,954 cell colors by Th17 cell types. Gray circle: DA Th17 cells in REOLP. f Left, dot plot of the IC from TREM1 + Mφ to naïve CD4 + T cells in IL1 signaling pathway in the inflammatory development of oral mucosal epithelium. Dot size, p-value; color scale, IC probability. Right, the developmental trajectory of T cell subtypes. g Bar plot exhibiting the upregulated signaling pathways of pathogenic Th17 cells in the inflammatory development of oral mucosal epithelium.

    Article Snippet: The primary antibodies included GSDMD (1:1000; Bioss, China, #BS-14287R), TREM1 (1:600; Proteintech, China, #11791-1-AP), and β-Actin (1:2000; Cell Signaling, U.S., #4970S).

    Techniques: Expressing, Quantitative Proteomics, Protein-Protein interactions

    a Spatial scatter plot of tissue zones (left) and spatial distribution of cell types (right) in the inflammatory development of oral mucosal epithelium. b Spatial intercellular communication of different samples in the inflammatory development of oral mucosal epithelium. c Histogram showing the spot proportions of cell types in epithelial regions (left) and immune regions (right) during the inflammatory development of oral mucosal epithelium. d Barplots showing the upregulated signaling pathways of pyroptotic epithelial cell regions (left), TREM1 + Mφ regions (middle), and pathogenic Th17 cell regions (right) during the inflammatory development of oral mucosal epithelium.

    Journal: Cell Death Discovery

    Article Title: Epithelial pyroptosis-induced TREM1 + macrophages activate Th17 cells to accelerate oral mucosal inflammation

    doi: 10.1038/s41420-025-02853-7

    Figure Lengend Snippet: a Spatial scatter plot of tissue zones (left) and spatial distribution of cell types (right) in the inflammatory development of oral mucosal epithelium. b Spatial intercellular communication of different samples in the inflammatory development of oral mucosal epithelium. c Histogram showing the spot proportions of cell types in epithelial regions (left) and immune regions (right) during the inflammatory development of oral mucosal epithelium. d Barplots showing the upregulated signaling pathways of pyroptotic epithelial cell regions (left), TREM1 + Mφ regions (middle), and pathogenic Th17 cell regions (right) during the inflammatory development of oral mucosal epithelium.

    Article Snippet: The primary antibodies included GSDMD (1:1000; Bioss, China, #BS-14287R), TREM1 (1:600; Proteintech, China, #11791-1-AP), and β-Actin (1:2000; Cell Signaling, U.S., #4970S).

    Techniques: Protein-Protein interactions

    a Flow chart of the establishment of the clinical follow-up cohort. b Top, radar plot of cell type fraction in the inflammatory development of oral mucosal epithelium based on BayesPrism deconvolution. Bottom, barplot of the upregulated signaling pathways in the REOLP through ssGSEA. c Box plots show the expression of cell markers in the inflammatory development of oral mucosal epithelium. d Density plots exhibiting the correlation of cell markers in pyroptotic epithelial cells, TREM1 + Mφ, and pathogenic Th17 cells in the inflammatory development of oral mucosal epithelium. Red: REOLP. Blue: NREOLP. e Univariate logistic regression model revealing the risk factors of the inflammatory development of oral mucosal epithelium. f PCA biplot of marker gene expression. Arrows represent gene loading vectors, colored by contribution magnitude (contribution 12–16; color bar). g Scree plot of condition indices for collinearity diagnostics. Horizontal dashed lines indicate thresholds for severe (red, >30) and moderate (orange, >15) multicollinearity.

    Journal: Cell Death Discovery

    Article Title: Epithelial pyroptosis-induced TREM1 + macrophages activate Th17 cells to accelerate oral mucosal inflammation

    doi: 10.1038/s41420-025-02853-7

    Figure Lengend Snippet: a Flow chart of the establishment of the clinical follow-up cohort. b Top, radar plot of cell type fraction in the inflammatory development of oral mucosal epithelium based on BayesPrism deconvolution. Bottom, barplot of the upregulated signaling pathways in the REOLP through ssGSEA. c Box plots show the expression of cell markers in the inflammatory development of oral mucosal epithelium. d Density plots exhibiting the correlation of cell markers in pyroptotic epithelial cells, TREM1 + Mφ, and pathogenic Th17 cells in the inflammatory development of oral mucosal epithelium. Red: REOLP. Blue: NREOLP. e Univariate logistic regression model revealing the risk factors of the inflammatory development of oral mucosal epithelium. f PCA biplot of marker gene expression. Arrows represent gene loading vectors, colored by contribution magnitude (contribution 12–16; color bar). g Scree plot of condition indices for collinearity diagnostics. Horizontal dashed lines indicate thresholds for severe (red, >30) and moderate (orange, >15) multicollinearity.

    Article Snippet: The primary antibodies included GSDMD (1:1000; Bioss, China, #BS-14287R), TREM1 (1:600; Proteintech, China, #11791-1-AP), and β-Actin (1:2000; Cell Signaling, U.S., #4970S).

    Techniques: Protein-Protein interactions, Expressing, Marker, Gene Expression

    a Flow chart of cytological experiments. b Flow cytometry showing the TREM1 expression of the TREM1 + Mφ and TREM1 NC Mφ. c Elisa assay depicting the concentration of IL-1β in TREM1 + Mφ and TREM1 NC Mφ with/without the stimulation of recombinant human HMGB1 (rhHMGB1), respectively. Note: ** p < 0.01, NS not statistically significant. Flow cytometry ( d ) and statistical analysis ( e ) of the c e ll proportion of CD4 + IL-17A + cells, CD4 + IL-17F + cells, and CD4 + IL-22 + cells after murine naïve CD4 + T cells co - cultured with the supernatants of TREM1 + Mφ, IL-6 and IL-23, with/without neutralizing anti-IL-1β (α-IL-1β). Note: * p < 0.05, ** p < 0.01, NS not statistically significant. f Representative images of mIHC in NREOLP (top) and REOLP (bottom). Scale bars: 100 µM (top) and 50 µM (bottom). Yellow arrows pointed to LPS + GSDMD + E-cad + cells. Red arrows pointed to TREM1 + CD68 + cells. Green arrows pointed to IL-17A + CD3 + cells.

    Journal: Cell Death Discovery

    Article Title: Epithelial pyroptosis-induced TREM1 + macrophages activate Th17 cells to accelerate oral mucosal inflammation

    doi: 10.1038/s41420-025-02853-7

    Figure Lengend Snippet: a Flow chart of cytological experiments. b Flow cytometry showing the TREM1 expression of the TREM1 + Mφ and TREM1 NC Mφ. c Elisa assay depicting the concentration of IL-1β in TREM1 + Mφ and TREM1 NC Mφ with/without the stimulation of recombinant human HMGB1 (rhHMGB1), respectively. Note: ** p < 0.01, NS not statistically significant. Flow cytometry ( d ) and statistical analysis ( e ) of the c e ll proportion of CD4 + IL-17A + cells, CD4 + IL-17F + cells, and CD4 + IL-22 + cells after murine naïve CD4 + T cells co - cultured with the supernatants of TREM1 + Mφ, IL-6 and IL-23, with/without neutralizing anti-IL-1β (α-IL-1β). Note: * p < 0.05, ** p < 0.01, NS not statistically significant. f Representative images of mIHC in NREOLP (top) and REOLP (bottom). Scale bars: 100 µM (top) and 50 µM (bottom). Yellow arrows pointed to LPS + GSDMD + E-cad + cells. Red arrows pointed to TREM1 + CD68 + cells. Green arrows pointed to IL-17A + CD3 + cells.

    Article Snippet: The primary antibodies included GSDMD (1:1000; Bioss, China, #BS-14287R), TREM1 (1:600; Proteintech, China, #11791-1-AP), and β-Actin (1:2000; Cell Signaling, U.S., #4970S).

    Techniques: Flow Cytometry, Expressing, Enzyme-linked Immunosorbent Assay, Concentration Assay, Recombinant, Cell Culture

    A Schematic of the establishment of the ORGUAMIA database. The role of epithelial pyroptosis-induced TREM1 + Mφ in periodontitis (PD) datasets ( B ) and IBD datasets ( C ). Left, UMAP plot of cell colors by cell types, myeloid cell types, and epithelial cell types. Middle, Histogram showing the cell proportions of myeloid cell types (top) and epithelial cell types with disease subtypes (bottom). Top right, violin plot showing the IL1B expression in Mφ subtype. Bottom right, circle plot of the intercellular communication from pyroptotic epithelial cells to other cells. Line width, the intercellular communication strength. Red arrow, the intercellular communication strength in PD/IBD was higher than in normal. Blue arrow, the intercellular communication strength in normal was higher than in PD/IBD.

    Journal: Cell Death Discovery

    Article Title: Epithelial pyroptosis-induced TREM1 + macrophages activate Th17 cells to accelerate oral mucosal inflammation

    doi: 10.1038/s41420-025-02853-7

    Figure Lengend Snippet: A Schematic of the establishment of the ORGUAMIA database. The role of epithelial pyroptosis-induced TREM1 + Mφ in periodontitis (PD) datasets ( B ) and IBD datasets ( C ). Left, UMAP plot of cell colors by cell types, myeloid cell types, and epithelial cell types. Middle, Histogram showing the cell proportions of myeloid cell types (top) and epithelial cell types with disease subtypes (bottom). Top right, violin plot showing the IL1B expression in Mφ subtype. Bottom right, circle plot of the intercellular communication from pyroptotic epithelial cells to other cells. Line width, the intercellular communication strength. Red arrow, the intercellular communication strength in PD/IBD was higher than in normal. Blue arrow, the intercellular communication strength in normal was higher than in PD/IBD.

    Article Snippet: The primary antibodies included GSDMD (1:1000; Bioss, China, #BS-14287R), TREM1 (1:600; Proteintech, China, #11791-1-AP), and β-Actin (1:2000; Cell Signaling, U.S., #4970S).

    Techniques: Expressing

    a Flow chart of cytological experiments. b Flow cytometry showing the TREM1 expression of the TREM1 + Mφ and TREM1 NC Mφ. c Elisa assay depicting the concentration of IL-1β in TREM1 + Mφ and TREM1 NC Mφ with/without the stimulation of recombinant human HMGB1 (rhHMGB1), respectively. Note: ** p < 0.01, NS not statistically significant. Flow cytometry ( d ) and statistical analysis ( e ) of the c e ll proportion of CD4 + IL-17A + cells, CD4 + IL-17F + cells, and CD4 + IL-22 + cells after murine naïve CD4 + T cells co - cultured with the supernatants of TREM1 + Mφ, IL-6 and IL-23, with/without neutralizing anti-IL-1β (α-IL-1β). Note: * p < 0.05, ** p < 0.01, NS not statistically significant. f Representative images of mIHC in NREOLP (top) and REOLP (bottom). Scale bars: 100 µM (top) and 50 µM (bottom). Yellow arrows pointed to LPS + GSDMD + E-cad + cells. Red arrows pointed to TREM1 + CD68 + cells. Green arrows pointed to IL-17A + CD3 + cells.

    Journal: Cell Death Discovery

    Article Title: Epithelial pyroptosis-induced TREM1 + macrophages activate Th17 cells to accelerate oral mucosal inflammation

    doi: 10.1038/s41420-025-02853-7

    Figure Lengend Snippet: a Flow chart of cytological experiments. b Flow cytometry showing the TREM1 expression of the TREM1 + Mφ and TREM1 NC Mφ. c Elisa assay depicting the concentration of IL-1β in TREM1 + Mφ and TREM1 NC Mφ with/without the stimulation of recombinant human HMGB1 (rhHMGB1), respectively. Note: ** p < 0.01, NS not statistically significant. Flow cytometry ( d ) and statistical analysis ( e ) of the c e ll proportion of CD4 + IL-17A + cells, CD4 + IL-17F + cells, and CD4 + IL-22 + cells after murine naïve CD4 + T cells co - cultured with the supernatants of TREM1 + Mφ, IL-6 and IL-23, with/without neutralizing anti-IL-1β (α-IL-1β). Note: * p < 0.05, ** p < 0.01, NS not statistically significant. f Representative images of mIHC in NREOLP (top) and REOLP (bottom). Scale bars: 100 µM (top) and 50 µM (bottom). Yellow arrows pointed to LPS + GSDMD + E-cad + cells. Red arrows pointed to TREM1 + CD68 + cells. Green arrows pointed to IL-17A + CD3 + cells.

    Article Snippet: The primary antibodies included were GSDMD (1:500; Bioss, China; #BS-14287R), E-cadherin (1:1000; HUABIO, China; #ET1607-75), LPS (1:100; Cloud-clone, China; MAB526Ge22), TREM1 (1:1000; Proteintech, China; #11791-1-AP), CD68 (1:200; Abcam, England; #ab201340), IL-17A (1:300; Proteintech, China; #26163-AP), CD3 (1:1000; HUABIO, China; #HA720082), and DAPI (1:500; Beyotime, China; #C1002).

    Techniques: Flow Cytometry, Expressing, Enzyme-linked Immunosorbent Assay, Concentration Assay, Recombinant, Cell Culture