anti trem1  (R&D Systems)

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

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

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

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

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

Journal: Journal of Neuroinflammation

Article Title: HIV gp120 induces TREM1 expression through TLR–PGE₂ signalling in human monocyte-derived microglia

doi: 10.1186/s12974-026-03757-8

Figure Lengend Snippet: HIV Ba−L gp120 increases expression of BCL2, BCLXL, and TREM1 in microglia. A MMG were treated with gp120 or vehicle. After 24 h, cells were harvested and assayed for BCL2, BCLXL, BAX, BAD, and TREM1 expression. Left: representative western blots with ACTB as loading control. Right: densitometric analysis ( n = 4). B gp120 (2 ng mL⁻¹), LPS (100 ng mL⁻¹), or vehicle were pre-incubated for 1 h at 37 °C with 1 mM 2-sulphanylethan-1-ol (2-Me), 5 µg mL⁻¹ anti-gp120 antibody (VRC01), or 5 µg mL⁻¹ isotype control IgG. After 24 h treatment, TNF and IL-10 levels were quantified by ELISA ( n = 4). Dashed lines denote the assay limit of detection. C gp120 was pre-incubated with 5 µg mL⁻¹ VRC01 or isotype IgG for 1 h at 37 °C, then added to MMG. TREM1 expression was assessed by western blot at 24 h. Left: representative blots; right: densitometry ( n = 4). D MMG were transfected with TREM1 siRNA (si TREM1 ) or scrambled siRNA (siNS) for 48 h, followed by gp120 or vehicle treatment for 24 h. BCL2, BCLXL, BAX, BAD, and TREM1 were analysed by western blot. Left: representative western blots with ACTB as loading control; right: densitometry ( n = 4). The inset ‘% TREM remaining’ represents TREM1/ACTB densitometry expressed relative to the untreated siNS condition (set to 100%). E Cells from (D) were fixed, permeabilised, and assayed for apoptotic ssDNA by ELISA as a marker of apoptosis ( n = 4). F Supernatants from (D) were analysed for lactate dehydrogenase (LDH) activity as a marker of cytotoxicity ( n = 4). Individual data points represent biological replicates; bars indicate mean ± SD. * p < 0.05

Article Snippet: Quantitative polymerase chain reaction (qPCR) was conducted using an Applied Biosystems QuantStudio 384-well real-time qPCR system with TaqMan Fast Advanced Master Mix and commercially available probes targeting PTGES (Hs00610420_m1; FAM-MGB), PTGES3 (Hs04187819_g1; FAM-MGB), PTGS1 (Hs00377726_m1; FAM-MGB), PTGS2 (Hs00153133_m1; FAM-MGB), and TREM1 (Hs00218624_m1; FAM-MGB), as well as the reference gene POLR2A (Hs00172187_m1; VIC-MGB), all from Applied Biosystems.

Techniques: Expressing, Western Blot, Control, Incubation, Enzyme-linked Immunosorbent Assay, Transfection, Marker, Activity Assay

Journal: Journal of Neuroinflammation

Article Title: HIV gp120 induces TREM1 expression through TLR–PGE₂ signalling in human monocyte-derived microglia

doi: 10.1186/s12974-026-03757-8

Figure Lengend Snippet: HIV Ba−L gp120-mediated TREM1 expression in microglia is dependent on TLR2 and TLR4 but not CCR5. A MMG were transfected with siRNA targeting TLR2 (si TLR2 ), TLR4 (si TLR4 ), or scrambled control (siNS) for 48 h, then treated with gp120 or vehicle for 24 h. Left: representative western blots for TLR2, TLR4, and TREM1, with ACTB as loading control. Right: densitometric quantification ( n = 4). B MMG were transfected with scrambled siRNA (siNS) or combined siRNAs targeting TLR2 and TLR4 (si TLR2 & si TLR4 ) for 48 h, pretreated with maraviroc (10 nM) or vehicle for 1 h, and then exposed to gp120 (2 ng mL⁻¹) or vehicle for 24 h. TREM1 protein levels were assessed by western blot (left) and quantified by densitometry (right; n = 4). C MMG were transfected with scrambled siRNA (siNC) or siRNA targeting CCR5 (si CCR5 ) for 48 h, followed by exposure to gp120 (2 ng mL⁻¹) or vehicle for 24 h. Left: representative western blots for CCR5 and TREM1 with ACTB as loading control. Right: densitometric quantification confirming effective CCR5 knockdown and preserved gp120-induced TREM1 upregulation ( n = 4). TREM1 and ACTB in this panel were detected using antibody clones distinct from those used in other figures (see Methods). Data are shown as mean ± SD; * p < 0.05

Article Snippet: Quantitative polymerase chain reaction (qPCR) was conducted using an Applied Biosystems QuantStudio 384-well real-time qPCR system with TaqMan Fast Advanced Master Mix and commercially available probes targeting PTGES (Hs00610420_m1; FAM-MGB), PTGES3 (Hs04187819_g1; FAM-MGB), PTGS1 (Hs00377726_m1; FAM-MGB), PTGS2 (Hs00153133_m1; FAM-MGB), and TREM1 (Hs00218624_m1; FAM-MGB), as well as the reference gene POLR2A (Hs00172187_m1; VIC-MGB), all from Applied Biosystems.

Techniques: Expressing, Transfection, Control, Western Blot, Knockdown, Clone Assay

Journal: Journal of Neuroinflammation

Article Title: HIV gp120 induces TREM1 expression through TLR–PGE₂ signalling in human monocyte-derived microglia

doi: 10.1186/s12974-026-03757-8

Figure Lengend Snippet: HIV Ba−L gp120 induces PGE 2 expression in microglia via PTGS2 and PTGES. A–C MMG were pretreated with 10 nM SC560, 100 nM celecoxib, or vehicle for 1 h, then exposed to 2 ng mL⁻¹ gp120 or vehicle ( n = 4). A After 24 h, PGE₂ levels were measured by competitive immunoassay. B TREM1 mRNA was quantified at 6 h by RT-qPCR. C TREM1 protein was quantified at 24 h by western blot. Left: representative blots with ACTB as loading control. Right: densitometric analysis ( n = 4). D–F MMG were pretreated with 100 nM MF63 or vehicle for 1 h, then treated with gp120 or vehicle ( n = 4). D PGE₂ was measured at 24 h. E TREM1 protein was quantified at 24 h by western blot. Left: representative blots with ACTB as loading control. Right: densitometric analysis ( n = 4). G MMG were treated with gp120 or vehicle and harvested at multiple time points. PTGS2 and TREM1 mRNA were assessed by RT-qPCR, and PGE₂ by immunoassay ( n = 4). H Conditioned media were collected at early and late time points following gp120 or vehicle exposure and analysed for extracellular WARS1 by ELISA, with non-zero time points plotted on a log 10 time scale ( n = 4). I MMG were treated with PGE₂ or vehicle. TREM1 mRNA was measured at 6 h ( n = 4). J MMG were pretreated with 100 nM SC51322 (PTGER1/EP1 antagonist), 100 nM PF 04418948 (PTGER2/EP2 antagonist), 100 nM L-798,106 (PTGER3/EP3 antagonist), 100 nM E7046 (PTGER4/EP4 antagonist), or vehicle for 1 h before gp120 or vehicle exposure. TREM1 mRNA was quantified at 6 h by RT-qPCR ( n = 4). Data are shown as mean ± SD; * p < 0.05

Article Snippet: Quantitative polymerase chain reaction (qPCR) was conducted using an Applied Biosystems QuantStudio 384-well real-time qPCR system with TaqMan Fast Advanced Master Mix and commercially available probes targeting PTGES (Hs00610420_m1; FAM-MGB), PTGES3 (Hs04187819_g1; FAM-MGB), PTGS1 (Hs00377726_m1; FAM-MGB), PTGS2 (Hs00153133_m1; FAM-MGB), and TREM1 (Hs00218624_m1; FAM-MGB), as well as the reference gene POLR2A (Hs00172187_m1; VIC-MGB), all from Applied Biosystems.

Techniques: Expressing, Quantitative RT-PCR, Western Blot, Control, Enzyme-linked Immunosorbent Assay

Journal: Journal of Neuroinflammation

Article Title: HIV gp120 induces TREM1 expression through TLR–PGE₂ signalling in human monocyte-derived microglia

doi: 10.1186/s12974-026-03757-8

Figure Lengend Snippet: HIV Ba−L gp120-mediated TREM1 expression in microglia depends on Ca 2+ -regulated PGE 2 synthesis. MMG were pretreated with 2 mM EGTA or vehicle for 1 h before exposure to gp120 or vehicle ( n = 4). A After 6 h, cells were analysed for PTGS2 , PTGES , and TREM1 mRNA by RT-qPCR. B At 24 h, cells were harvested and analysed by western blot for PTGS2, PTGES, and TREM1; ACTB was used as a loading control. Left: representative blots. Right: densitometric analysis ( n = 4). C Supernatants were assessed for PGE₂ content by competitive enzyme immunoassay. D TNF and IL-10 release were quantified by ELISA; dashed lines indicate assay detection limits. Data are shown as mean ± SD; * p < 0.05

Article Snippet: Quantitative polymerase chain reaction (qPCR) was conducted using an Applied Biosystems QuantStudio 384-well real-time qPCR system with TaqMan Fast Advanced Master Mix and commercially available probes targeting PTGES (Hs00610420_m1; FAM-MGB), PTGES3 (Hs04187819_g1; FAM-MGB), PTGS1 (Hs00377726_m1; FAM-MGB), PTGS2 (Hs00153133_m1; FAM-MGB), and TREM1 (Hs00218624_m1; FAM-MGB), as well as the reference gene POLR2A (Hs00172187_m1; VIC-MGB), all from Applied Biosystems.

Techniques: Expressing, Quantitative RT-PCR, Western Blot, Control, Enzyme-linked Immunosorbent Assay

Journal: Journal of Neuroinflammation

Article Title: HIV gp120 induces TREM1 expression through TLR–PGE₂ signalling in human monocyte-derived microglia

doi: 10.1186/s12974-026-03757-8

Figure Lengend Snippet: HIV Ba−L gp120-mediated TREM1 expression in microglia depends on CAMKII and calcineurin–NFAT signalling. A–D Monocyte-derived microglia (MMG) were pretreated with 10 ng mL⁻¹ tacrolimus, 1 µM KN93, or vehicle for 1 h, then treated with gp120 or vehicle ( n = 4). A After 6 h, cells were analysed for PTGS2 , PTGES , and TREM1 mRNA by RT-qPCR. B At 24 h, lysates were analysed by western blot for PTGS2, PTGES, and TREM1; ACTB was used as a loading control. Top: representative blots. Bottom: densitometric analysis ( n = 4). C Supernatants were assessed for PGE₂ by competitive enzyme immunoassay. D TNF and IL-10 were measured by ELISA; dashed lines indicate assay detection limits. E–F MMG were treated with gp120 or vehicle for 6 h. E Western blot analysis for Ser172-phosphorylated NFATC1, total NFATC1, and ACTB (loading control). Representative blots shown ( n = 4). F Cytoplasmic and nuclear fractions analysed for NFATC1, with ACTB (cytoplasmic) and H3C1 (nuclear) as loading controls. Representative blots shown ( n = 4). Data are shown as mean ± SD; * p < 0.05

Article Snippet: Quantitative polymerase chain reaction (qPCR) was conducted using an Applied Biosystems QuantStudio 384-well real-time qPCR system with TaqMan Fast Advanced Master Mix and commercially available probes targeting PTGES (Hs00610420_m1; FAM-MGB), PTGES3 (Hs04187819_g1; FAM-MGB), PTGS1 (Hs00377726_m1; FAM-MGB), PTGS2 (Hs00153133_m1; FAM-MGB), and TREM1 (Hs00218624_m1; FAM-MGB), as well as the reference gene POLR2A (Hs00172187_m1; VIC-MGB), all from Applied Biosystems.

Techniques: Expressing, Derivative Assay, Quantitative RT-PCR, Western Blot, Control, Enzyme-linked Immunosorbent Assay

Journal: Journal of Neuroinflammation

Article Title: HIV gp120 induces TREM1 expression through TLR–PGE₂ signalling in human monocyte-derived microglia

doi: 10.1186/s12974-026-03757-8

Figure Lengend Snippet: HIV Ba−L gp120-mediated PGE 2 expression in microglia is independent of NF-κB. Monocyte-derived microglia (MMG) were transfected with RELA siRNA (si RELA ), NFATC1 siRNA (si NFATC1 ), or scrambled siRNA (siNS) for 48 h, followed by treatment with gp120 or vehicle for 24 h ( n = 4). A Left: representative western blots of RELA, NFATC1, TREM1, PTGS2, and PTGES with ACTB as a loading control. Right: densitometric analysis of blots. B Supernatants were analysed for PGE₂ by competitive enzyme immunoassay. Data are shown as mean ± SD

Article Snippet: Quantitative polymerase chain reaction (qPCR) was conducted using an Applied Biosystems QuantStudio 384-well real-time qPCR system with TaqMan Fast Advanced Master Mix and commercially available probes targeting PTGES (Hs00610420_m1; FAM-MGB), PTGES3 (Hs04187819_g1; FAM-MGB), PTGS1 (Hs00377726_m1; FAM-MGB), PTGS2 (Hs00153133_m1; FAM-MGB), and TREM1 (Hs00218624_m1; FAM-MGB), as well as the reference gene POLR2A (Hs00172187_m1; VIC-MGB), all from Applied Biosystems.

Techniques: Expressing, Derivative Assay, Transfection, Western Blot, Control, Enzyme-linked Immunosorbent Assay

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: TREM1 inhibitory peptide GF9 (MCE, HY- P10086 ) and LP17 (MCE, HY-P3400).

Techniques: Derivative Assay, Functional Assay, Expressing, Immunostaining

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: TREM1 inhibitory peptide GF9 (MCE, HY- P10086 ) and LP17 (MCE, HY-P3400).

Techniques: Reverse Transcription, Mutagenesis, Derivative Assay

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: TREM1 inhibitory peptide GF9 (MCE, HY- P10086 ) and LP17 (MCE, HY-P3400).

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

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: TREM1 inhibitory peptide GF9 (MCE, HY- P10086 ) and LP17 (MCE, HY-P3400).

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

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: TREM1 inhibitory peptide GF9 (MCE, HY- P10086 ) and LP17 (MCE, HY-P3400).

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

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

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

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

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