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cd45 (til) microbeads, mouse  (Miltenyi Biotec)


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    Miltenyi Biotec cd45 (til) microbeads, mouse
    Cd45 (Til) Microbeads, Mouse, supplied by Miltenyi Biotec, used in various techniques. Bioz Stars score: 96/100, based on 134 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/mouse+cd45+til+microbeads/CD45+(TIL)+MicroBeads%2C+mouse/custom%40130-110-618%4042476286
    Average 96 stars, based on 134 article reviews
    cd45 (til) microbeads, mouse - by Bioz Stars, 2026-10
    96/100 stars

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    Isolation:

    Article Title: Microbiome-derived hydroxyphenyl propanoates enhance antitumour immunity by potentiating gasdermin D activity in tumour-associated myeloid cells
    Article Snippet: Single-cell suspensions were prepared using Mouse Tumour Dissociation Kit (Miltenyi Biotec). .. Viable cells were enriched using Dead Cell Removal Kit (130-090-101; Miltenyi Biotec), and CD45 + tumour-infiltrating immune cells were isolated using Mouse CD45 (TIL) Microbeads (130-110-618; Miltenyi Biotec). ..

    Article Title: Improved antitumor effectiveness of oncolytic HSV-1 viruses engineered with IL-15/IL-15Rα complex combined with oncolytic HSV-1-aPD1 targets colon cancer.
    Article Snippet: Tumor single-cell suspensions were prepared using the Tumor Dissociation Kit (Miltenyi Biotec, Gladbach, Germany), followed by removal of dead cells using the Dead Cell Removal Kit (Miltenyi Biotec, Germany). .. CD45+ tumor-infiltrating leukocytes were isolated using mouse CD45+ TIL Microbeads (Miltenyi Biotec, Germany). .. CT26.WT cells were pre-labeled with Carboxifluorescein diacetate N-succinimidyl ester (CSFE) (Biolegend, USA) as target cells.

    Article Title: Dual-antigen Doggybone TM DNA vaccine induces potent anti-tumor immunity against immunosuppressive oral cancer
    Article Snippet: Tumors were harvested and processed using the Mouse Tumor Dissociation Kit (Miltenyi Biotec, 130-096-730) and the gentleMACS Dissociator (Miltenyi Biotec) following the manufacturer’s protocol. .. CD45 + TILs were isolated using Mouse CD45 TIL MicroBeads (Miltenyi Biotec, 130-110-618). ..

    Article Title: Improved antitumor effectiveness of oncolytic HSV-1 viruses engineered with IL-15/IL-15Rα complex combined with oncolytic HSV-1-aPD1 targets colon cancer
    Article Snippet: Tumor single-cell suspensions were prepared using the Tumor Dissociation Kit (Miltenyi Biotec, Gladbach, Germany), followed by removal of dead cells using the Dead Cell Removal Kit (Miltenyi Biotec, Germany). .. CD45 + tumor-infiltrating leukocytes were isolated using mouse CD45 + TIL Microbeads (Miltenyi Biotec, Germany). .. CT26.WT cells were pre-labeled with Carboxifluorescein diacetate N-succinimidyl ester (CSFE) (Biolegend, USA) as target cells.

    Article Title: Enhancing immune response and survival in hepatocellular carcinoma with novel oncolytic Jurona virus and immune checkpoint blockade.
    Article Snippet: Analysis of tumor-infiltrating immune cells Hepa 1–6 tumors (n = 3 samples/group) were excised and dissociated on day 18, 3 days after the last JURV injection, using a mouse tumor dissociation kit (Miltenyi, cat. no. 130-096-730) with a gentleMACS Octo Dissociator (Miltenyi) according to themanufacturer’s protocol. .. CD45+ cells were isolated with mouse CD45 (TIL) microbeads (Miltenyi). .. Cells were incubated with Fixable Viability Stain 510 for 15 min at 4 C, followed by anti-Fc blocking reagent (BioLegend, cat. no. 101320) for 10 min before surface staining.

    Article Title: Enhancing immune response and survival in hepatocellular carcinoma with novel oncolytic Jurona virus and immune checkpoint blockade
    Article Snippet: Hepa 1–6 tumors ( n = 3 samples/group) were excised and dissociated on day 18, 3 days after the last JURV injection, using a mouse tumor dissociation kit (Miltenyi, cat. no. 130-096-730) with a gentleMACS Octo Dissociator (Miltenyi) according to the manufacturer’s protocol. .. CD45 + cells were isolated with mouse CD45 (TIL) microbeads (Miltenyi). .. Cells were incubated with Fixable Viability Stain 510 for 15 min at 4°C, followed by anti-Fc blocking reagent (BioLegend, cat. no. 101320) for 10 min before surface staining.

    Lysis:

    Article Title: Selective depletion of CCR8+Treg cells enhances anti-tumor immunity of cytotoxic T cells in lung cancer via dendritic cells.
    Article Snippet: This is a PDF file of an article that has undergone enhancements after acceptance, such as the addition of a cover page and metadata, and formatting for readability, but it is not yet the definitive version of record.. This version will undergo additional copyediting, typesetting and review before it is published in its final form, but we are providing this version to give early visibility of the article.. Please note that, during the production process, errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.



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    Miltenyi Biotec cd45 (til) microbeads, mouse
    Cd45 (Til) Microbeads, Mouse, supplied by Miltenyi Biotec, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Miltenyi Biotec cd45 positive cells
    (A) Representative images (left panel) and quantification (right panel) of p16 + cancer cells in treatment-naive (n=17) and gemcitabine/cisplatin (Gem/Cis)-treated (n=22) human CCA. (B) Telomere-associated foci (γH2AX immunofluorescence with telomere fluorescence in situ hybridization) (left panel) and quantification (right panel) in p16 + cancer cells. (C-E) Sequential immunofluorescence quantifying p16 + cancer cells (KRT19 + ), cancer-associated fibroblasts (α-SMA + ), and immune cells <t>(CD45</t> + ), and the proliferative status (Ki67) of p16 + cells. (F) Senescence-associated β-galactosidase activity in human RBE CCA cells, proliferating versus doxorubicin or Gem/Cis-induced. (G) Single-nucleus RNA sequencing of human CCA (n=10 patients): UMAP of cell populations and expression of CDKN2A , CDKN1A , and MKI67 with senescence (SenMayo, Fridman, and Reactome cellular senescence) gene-set scores. (H) Multivariable Cox regression of senescence transcriptional scores and overall survival, adjusted for age, sex, and stage, performed independently in the Mayo discovery cohort (n=158, 108 events) and an external Asian cohort (OEP00105, n=244, 99 events). White arrows, senescent-like cancer cells. Scale bar, 50 µm. Data are mean ± SEM; *, P<0.05; **, P<0.01; ***, P<0.001; ****, P<0.0001; ns, not significant.
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    Miltenyi Biotec cd45 microbeads
    (A) Representative images (left panel) and quantification (right panel) of p16 + cancer cells in treatment-naive (n=17) and gemcitabine/cisplatin (Gem/Cis)-treated (n=22) human CCA. (B) Telomere-associated foci (γH2AX immunofluorescence with telomere fluorescence in situ hybridization) (left panel) and quantification (right panel) in p16 + cancer cells. (C-E) Sequential immunofluorescence quantifying p16 + cancer cells (KRT19 + ), cancer-associated fibroblasts (α-SMA + ), and immune cells <t>(CD45</t> + ), and the proliferative status (Ki67) of p16 + cells. (F) Senescence-associated β-galactosidase activity in human RBE CCA cells, proliferating versus doxorubicin or Gem/Cis-induced. (G) Single-nucleus RNA sequencing of human CCA (n=10 patients): UMAP of cell populations and expression of CDKN2A , CDKN1A , and MKI67 with senescence (SenMayo, Fridman, and Reactome cellular senescence) gene-set scores. (H) Multivariable Cox regression of senescence transcriptional scores and overall survival, adjusted for age, sex, and stage, performed independently in the Mayo discovery cohort (n=158, 108 events) and an external Asian cohort (OEP00105, n=244, 99 events). White arrows, senescent-like cancer cells. Scale bar, 50 µm. Data are mean ± SEM; *, P<0.05; **, P<0.01; ***, P<0.001; ****, P<0.0001; ns, not significant.
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    Miltenyi Biotec cd45 til microbeads
    (A) Representative images (left panel) and quantification (right panel) of p16 + cancer cells in treatment-naive (n=17) and gemcitabine/cisplatin (Gem/Cis)-treated (n=22) human CCA. (B) Telomere-associated foci (γH2AX immunofluorescence with telomere fluorescence in situ hybridization) (left panel) and quantification (right panel) in p16 + cancer cells. (C-E) Sequential immunofluorescence quantifying p16 + cancer cells (KRT19 + ), cancer-associated fibroblasts (α-SMA + ), and immune cells <t>(CD45</t> + ), and the proliferative status (Ki67) of p16 + cells. (F) Senescence-associated β-galactosidase activity in human RBE CCA cells, proliferating versus doxorubicin or Gem/Cis-induced. (G) Single-nucleus RNA sequencing of human CCA (n=10 patients): UMAP of cell populations and expression of CDKN2A , CDKN1A , and MKI67 with senescence (SenMayo, Fridman, and Reactome cellular senescence) gene-set scores. (H) Multivariable Cox regression of senescence transcriptional scores and overall survival, adjusted for age, sex, and stage, performed independently in the Mayo discovery cohort (n=158, 108 events) and an external Asian cohort (OEP00105, n=244, 99 events). White arrows, senescent-like cancer cells. Scale bar, 50 µm. Data are mean ± SEM; *, P<0.05; **, P<0.01; ***, P<0.001; ****, P<0.0001; ns, not significant.
    Cd45 Til Microbeads, supplied by Miltenyi Biotec, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Miltenyi Biotec mouse 130 110 618
    (A) Representative images (left panel) and quantification (right panel) of p16 + cancer cells in treatment-naive (n=17) and gemcitabine/cisplatin (Gem/Cis)-treated (n=22) human CCA. (B) Telomere-associated foci (γH2AX immunofluorescence with telomere fluorescence in situ hybridization) (left panel) and quantification (right panel) in p16 + cancer cells. (C-E) Sequential immunofluorescence quantifying p16 + cancer cells (KRT19 + ), cancer-associated fibroblasts (α-SMA + ), and immune cells <t>(CD45</t> + ), and the proliferative status (Ki67) of p16 + cells. (F) Senescence-associated β-galactosidase activity in human RBE CCA cells, proliferating versus doxorubicin or Gem/Cis-induced. (G) Single-nucleus RNA sequencing of human CCA (n=10 patients): UMAP of cell populations and expression of CDKN2A , CDKN1A , and MKI67 with senescence (SenMayo, Fridman, and Reactome cellular senescence) gene-set scores. (H) Multivariable Cox regression of senescence transcriptional scores and overall survival, adjusted for age, sex, and stage, performed independently in the Mayo discovery cohort (n=158, 108 events) and an external Asian cohort (OEP00105, n=244, 99 events). White arrows, senescent-like cancer cells. Scale bar, 50 µm. Data are mean ± SEM; *, P<0.05; **, P<0.01; ***, P<0.001; ****, P<0.0001; ns, not significant.
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    Miltenyi Biotec cd45 immune cells
    Sarcoma growth and leukocyte infiltration in IL1R2-deficient mice. A–C, Tumor volume of transplantable FS6 ( A ), MN/MCA1 ( B ), and 3-MCA–induced sarcoma ( C ) in IL1R2-competent [ n = 7 ( A ), 18 ( B ), and 16 ( C )] and -deficient [ n = 7 ( A ), 19 ( B ), and 19 ( C )] mice. D, Volume and the number of lung metastasis 27 days after MN/MCA1 intramuscular injection in Il1r2 +/+ ( n = 20) and Il1r2 −/− ( n = 22) mice. E, Analysis by FACS of IL1R2 protein expression [MFI compared with fluorescence minus one (FMO)] in myeloid and lymphoid populations isolated from FS6-bearing WT mice ( n = 8–9). F and G, Frequency of IL1R2 + cells on total neutrophils ( F ) and Tregs ( G ) in healthy ( n = 6) and FS6-bearing mice ( n = 9). H and I, Analysis by FACS of myeloid population frequency on total immune cells <t>(CD45</t> + ; H ) or myeloid and lymphoid cell number normalized on tumor volume (mm 3 ; I ) in FS6-bearing Il1r2 +/+ [ n = 14 ( H ) and 11 ( I )] and Il1r2 −/− [ n = 12 ( H ) and 9–10 ( I )] mice. E–I, Cell populations were defined as follows: neutrophils (Nϕ, CD11b + Ly6G + ), monocytes (Mono., CD11b + Ly6G − Ly6C + ), macrophages (Mϕ, CD11b + Ly6G − F4/80 + ), conventional CD4 + T cells (Conv. CD4 + , TCRβ + CD4 + FOXP3 − ), Tregs (TCRβ + CD4 + FOXP3 + ), CD8 + T cells (TCRβ + CD8 + ), NK cells (NK1.1 + ), and B cells (CD19 + ). J, Representative images of immunofluorescence (IF) of neutrophils (Ly6G + ) and blood vessels (CD31 + ) in FS6 tumor tissues of Il1r2 +/+ and Il1r2 −/− mice. Scale bar, 1 mm (left images) or 200 μm (right images). K, Analysis by IF of neutrophil number normalized on tissue area (mm 2 ) in FS6 tumor tissues derived from Il1r2 +/+ ( n = 8) and Il1r2 −/− ( n = 6) mice. L–O, Analysis by FACS of frequency ( L and N ) or cell number normalized on tumor volume (mm 3 ; M and O ) of neutrophils, monocytes, macrophages ( L and M ), or alveolar macrophages (CD11b − SiglecF + ; N and O ) in MN/MCA1 primary tumors ( L and M ) or metastasis ( N and O ) in Il1r2 +/+ [ n = 9 ( L and M ) and 10 ( N and O )] and Il1r2 −/− [ n = 10 ( L and M ) and 12 ( N and O )] mice. Mean ± SEM. One representative experiment of six ( A ) or two pooled experiments ( B , H , I , N , and O ); one representative experiment of two ( C , L , and M ) or four pooled experiments ( D ); and one experiment ( C , E–G , J , and K ) performed. P values determinded by two-way ANOVA ( A and B ) and two-tailed Mann–Whitney U test ( C–I and K–O ). *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001. DAPI, 4′,6-diamidino-2-phenylindole.
    Cd45 Immune Cells, supplied by Miltenyi Biotec, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Miltenyi Biotec mouse cd45 til microbeads
    a, immune cell types in the TME identified through scRNAseq of <t>CD45</t> + cells isolated from orthotopically implanted M3-9-M OVA cells; b, number of immune cell types detected in M3-9-M OVA tumours through scRNAseq experiment (n = 2 pooled samples per experimental groups); c, number of significantly impacted genes obtained from pairwise comparisons (Wilcoxon rank sum test); d, circos plot of all significantly impacted genes, obtained from pairwise comparisons of all cell types measured, that overlap with each other through identical or shared pathways; e, bar graph of transcriptional regulators of 3,2-HPP impacted genes; f-m, NF-κB and IRF induction in mouse RAW-Dual™ cells and human THP1-Dual™ cells with different pathogen recognition receptor agonists in the presence of HPP metabolites (HI = heat inactivated, three combined experiments, error bars represent standard error, one-way ANOVA test).
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    Miltenyi Biotec mouse
    a, immune cell types in the TME identified through scRNAseq of <t>CD45</t> + cells isolated from orthotopically implanted M3-9-M OVA cells; b, number of immune cell types detected in M3-9-M OVA tumours through scRNAseq experiment (n = 2 pooled samples per experimental groups); c, number of significantly impacted genes obtained from pairwise comparisons (Wilcoxon rank sum test); d, circos plot of all significantly impacted genes, obtained from pairwise comparisons of all cell types measured, that overlap with each other through identical or shared pathways; e, bar graph of transcriptional regulators of 3,2-HPP impacted genes; f-m, NF-κB and IRF induction in mouse RAW-Dual™ cells and human THP1-Dual™ cells with different pathogen recognition receptor agonists in the presence of HPP metabolites (HI = heat inactivated, three combined experiments, error bars represent standard error, one-way ANOVA test).
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    Image Search Results


    (A) Representative images (left panel) and quantification (right panel) of p16 + cancer cells in treatment-naive (n=17) and gemcitabine/cisplatin (Gem/Cis)-treated (n=22) human CCA. (B) Telomere-associated foci (γH2AX immunofluorescence with telomere fluorescence in situ hybridization) (left panel) and quantification (right panel) in p16 + cancer cells. (C-E) Sequential immunofluorescence quantifying p16 + cancer cells (KRT19 + ), cancer-associated fibroblasts (α-SMA + ), and immune cells (CD45 + ), and the proliferative status (Ki67) of p16 + cells. (F) Senescence-associated β-galactosidase activity in human RBE CCA cells, proliferating versus doxorubicin or Gem/Cis-induced. (G) Single-nucleus RNA sequencing of human CCA (n=10 patients): UMAP of cell populations and expression of CDKN2A , CDKN1A , and MKI67 with senescence (SenMayo, Fridman, and Reactome cellular senescence) gene-set scores. (H) Multivariable Cox regression of senescence transcriptional scores and overall survival, adjusted for age, sex, and stage, performed independently in the Mayo discovery cohort (n=158, 108 events) and an external Asian cohort (OEP00105, n=244, 99 events). White arrows, senescent-like cancer cells. Scale bar, 50 µm. Data are mean ± SEM; *, P<0.05; **, P<0.01; ***, P<0.001; ****, P<0.0001; ns, not significant.

    Journal: bioRxiv

    Article Title: Therapy-induced senescent-like cancer cells drive macrophage-mediated immunosuppression in cholangiocarcinoma

    doi: 10.64898/2026.06.24.734341

    Figure Lengend Snippet: (A) Representative images (left panel) and quantification (right panel) of p16 + cancer cells in treatment-naive (n=17) and gemcitabine/cisplatin (Gem/Cis)-treated (n=22) human CCA. (B) Telomere-associated foci (γH2AX immunofluorescence with telomere fluorescence in situ hybridization) (left panel) and quantification (right panel) in p16 + cancer cells. (C-E) Sequential immunofluorescence quantifying p16 + cancer cells (KRT19 + ), cancer-associated fibroblasts (α-SMA + ), and immune cells (CD45 + ), and the proliferative status (Ki67) of p16 + cells. (F) Senescence-associated β-galactosidase activity in human RBE CCA cells, proliferating versus doxorubicin or Gem/Cis-induced. (G) Single-nucleus RNA sequencing of human CCA (n=10 patients): UMAP of cell populations and expression of CDKN2A , CDKN1A , and MKI67 with senescence (SenMayo, Fridman, and Reactome cellular senescence) gene-set scores. (H) Multivariable Cox regression of senescence transcriptional scores and overall survival, adjusted for age, sex, and stage, performed independently in the Mayo discovery cohort (n=158, 108 events) and an external Asian cohort (OEP00105, n=244, 99 events). White arrows, senescent-like cancer cells. Scale bar, 50 µm. Data are mean ± SEM; *, P<0.05; **, P<0.01; ***, P<0.001; ****, P<0.0001; ns, not significant.

    Article Snippet: CD45 positive cells were enriched with CD45 (TIL) MicroBeads, mouse (Miltenyi # 130-110-618) according to the manufacturer’s instruction.

    Techniques: Immunofluorescence, Fluorescence, In Situ Hybridization, Activity Assay, RNA Sequencing, Expressing

    (A) p21 + cancer cells in treatment-naive (n=15) versus Gem/Cis-treated (n=19) human CCA. (B-D) Sequential immunofluorescence of p21 + cancer cells (KRT19 + ), cancer-associated fibroblasts (α-SMA + ), and immune cells (CD45 + ), and Ki67 status. (E-F) Senescence induction in SB1 cells with alisertib (0.2 µM, Aurora kinase A inhibitor) or etoposide (0.5 µM, topoisomerase II inhibitor) over 6 days, with drug withdrawn at day 4, confirmed by SA-β-gal and (E) p21 immunostaining (F).

    Journal: bioRxiv

    Article Title: Therapy-induced senescent-like cancer cells drive macrophage-mediated immunosuppression in cholangiocarcinoma

    doi: 10.64898/2026.06.24.734341

    Figure Lengend Snippet: (A) p21 + cancer cells in treatment-naive (n=15) versus Gem/Cis-treated (n=19) human CCA. (B-D) Sequential immunofluorescence of p21 + cancer cells (KRT19 + ), cancer-associated fibroblasts (α-SMA + ), and immune cells (CD45 + ), and Ki67 status. (E-F) Senescence induction in SB1 cells with alisertib (0.2 µM, Aurora kinase A inhibitor) or etoposide (0.5 µM, topoisomerase II inhibitor) over 6 days, with drug withdrawn at day 4, confirmed by SA-β-gal and (E) p21 immunostaining (F).

    Article Snippet: CD45 positive cells were enriched with CD45 (TIL) MicroBeads, mouse (Miltenyi # 130-110-618) according to the manufacturer’s instruction.

    Techniques: Immunofluorescence, Immunostaining

    (A) SB1 p21-ATTAC in vivo study schematic. (B) Representative gross images and tumor-burden quantification, vehicle versus AP-treated SB1 p21-ATTAC tumors. (C) Relative mRNA of p21-promoter tGFP reporter in veh and AP treated murine SB1 p21-ATTAC tumors. (D) p21 mean fluorescence intensity in veh and AP treated murine SB1 p21-ATTAC tumors. Scale bar, 100 µm. (E) Body weights of SB1 p16-ATTAC tumor bearing mice treated with or AP. (F) Monocytic myeloid-derived suppressor cell (M-MDSC), polymorphonuclear myeloid-derived suppressor cell (PMN-MDSC), regulatory T-cell (Treg), CD4 + T cells, and natural killer (NK) frequencies (% of CD45 + cells) in in SB1 p16-ATTAC tumors. (G) M1 macrophage, TAM, CD8 + CTL, granzyme B + CD8 + CTL frequencies in SB1 p21-ATTAC tumors. (H) Body weights of SB1 p21-ATTAC tumor bearing mice treated with or AP. (I) M-MDSC, PMN-MDSC, Treg, CD4 + T-cell, and NK-cell frequencies in SB1 p21-ATTAC tumors. Data are mean ± SEM; *, P<0.05; **, P<0.01.

    Journal: bioRxiv

    Article Title: Therapy-induced senescent-like cancer cells drive macrophage-mediated immunosuppression in cholangiocarcinoma

    doi: 10.64898/2026.06.24.734341

    Figure Lengend Snippet: (A) SB1 p21-ATTAC in vivo study schematic. (B) Representative gross images and tumor-burden quantification, vehicle versus AP-treated SB1 p21-ATTAC tumors. (C) Relative mRNA of p21-promoter tGFP reporter in veh and AP treated murine SB1 p21-ATTAC tumors. (D) p21 mean fluorescence intensity in veh and AP treated murine SB1 p21-ATTAC tumors. Scale bar, 100 µm. (E) Body weights of SB1 p16-ATTAC tumor bearing mice treated with or AP. (F) Monocytic myeloid-derived suppressor cell (M-MDSC), polymorphonuclear myeloid-derived suppressor cell (PMN-MDSC), regulatory T-cell (Treg), CD4 + T cells, and natural killer (NK) frequencies (% of CD45 + cells) in in SB1 p16-ATTAC tumors. (G) M1 macrophage, TAM, CD8 + CTL, granzyme B + CD8 + CTL frequencies in SB1 p21-ATTAC tumors. (H) Body weights of SB1 p21-ATTAC tumor bearing mice treated with or AP. (I) M-MDSC, PMN-MDSC, Treg, CD4 + T-cell, and NK-cell frequencies in SB1 p21-ATTAC tumors. Data are mean ± SEM; *, P<0.05; **, P<0.01.

    Article Snippet: CD45 positive cells were enriched with CD45 (TIL) MicroBeads, mouse (Miltenyi # 130-110-618) according to the manufacturer’s instruction.

    Techniques: In Vivo, Fluorescence, Derivative Assay

    (A) Schema depicting in vivo study. SB tumor-bearing mice were treated for 2 weeks with vehicle, alisertib or etoposide. (B) Frequencies of M1 macrophages and M2-like tumor-associated macrophages (TAMs) (% of CD45 + cells) by flow cytometry. (C) Schematic of macrophage education; senescent-like state induced by alisertib or etoposide. (D) Bone-marrow-derived macrophage (BMDM) viability after conditioned medium from proliferating versus senescent-like cells. (E) Proliferation of CFSE-labeled CD8 + T cells co-cultured with educated BMDMs. Data are mean ± SEM; *, P<0.05; **, P<0.01; ***, P<0.001; ****, P<0.0001; ns, not significant.

    Journal: bioRxiv

    Article Title: Therapy-induced senescent-like cancer cells drive macrophage-mediated immunosuppression in cholangiocarcinoma

    doi: 10.64898/2026.06.24.734341

    Figure Lengend Snippet: (A) Schema depicting in vivo study. SB tumor-bearing mice were treated for 2 weeks with vehicle, alisertib or etoposide. (B) Frequencies of M1 macrophages and M2-like tumor-associated macrophages (TAMs) (% of CD45 + cells) by flow cytometry. (C) Schematic of macrophage education; senescent-like state induced by alisertib or etoposide. (D) Bone-marrow-derived macrophage (BMDM) viability after conditioned medium from proliferating versus senescent-like cells. (E) Proliferation of CFSE-labeled CD8 + T cells co-cultured with educated BMDMs. Data are mean ± SEM; *, P<0.05; **, P<0.01; ***, P<0.001; ****, P<0.0001; ns, not significant.

    Article Snippet: CD45 positive cells were enriched with CD45 (TIL) MicroBeads, mouse (Miltenyi # 130-110-618) according to the manufacturer’s instruction.

    Techniques: In Vivo, Flow Cytometry, Derivative Assay, Labeling, Cell Culture

    (A) M-MDSC, PMN-MDSC, and regulatory T-cell (Treg) frequencies (% of CD45 + cells) in the SB1 tumor bearing mice treated with vehicle, alisertib, or etoposide. (B) Schematic of subcutaneous tumor model study. (C) M1 macrophage, TAM, M-MDSC, PMN-MDSC, Treg frequencies in subcutaneous SB1 tumor bearing mice treated with vehicle, alisertib, or etoposide. Data are mean ± SEM; *, P<0.05; **; ns, not significant.

    Journal: bioRxiv

    Article Title: Therapy-induced senescent-like cancer cells drive macrophage-mediated immunosuppression in cholangiocarcinoma

    doi: 10.64898/2026.06.24.734341

    Figure Lengend Snippet: (A) M-MDSC, PMN-MDSC, and regulatory T-cell (Treg) frequencies (% of CD45 + cells) in the SB1 tumor bearing mice treated with vehicle, alisertib, or etoposide. (B) Schematic of subcutaneous tumor model study. (C) M1 macrophage, TAM, M-MDSC, PMN-MDSC, Treg frequencies in subcutaneous SB1 tumor bearing mice treated with vehicle, alisertib, or etoposide. Data are mean ± SEM; *, P<0.05; **; ns, not significant.

    Article Snippet: CD45 positive cells were enriched with CD45 (TIL) MicroBeads, mouse (Miltenyi # 130-110-618) according to the manufacturer’s instruction.

    Techniques:

    (A) Strategy for p16-promoter-restricted Gdf15 silencing (shRNA) and Gdf15 overexpression in orthotopic SB1 CCA. (B) Representative gross images (left) and tumor/liver weight quantification (right). (C-D) TAM and CD8 + CTL frequencies (% of CD45 + cells) in p16-shCtrl , SB-p16-shGdf15, and SB- p16-Gdf15 OE tumors via flow cytometry. (E) (A) EpCAM⁺GDF-15⁺ CCA cells (teal) adjacent to TAMs (pink); EpCAM⁺ (blue) and GDF-15⁺ (orange) transcripts shown. Scale bar 100 µm. (B) Per-TAM immunosuppressive score (per-sample z) versus distance to the nearest GDF-15⁺ or GDF-15⁻ CCA cell (TAMs ≤200 µm; n = 13,597 and 14,703 across three iCCA samples). Line/band: linear fit ± 95% CI; β and P from linear mixed-effects [score ∼ distance + (1|sample)]. The gradient is GDF-15⁺-specific (β = −3.79×10⁻³/µm, P < 10⁻¹⁰) and absent for GDF-15⁻ cells (β = +9.11×10⁻⁴/µm, P = 0.004). Scale bar, 100 µm. Data are mean ± SEM; *, P<0.05; ***, P<0.001; ns, not significant.

    Journal: bioRxiv

    Article Title: Therapy-induced senescent-like cancer cells drive macrophage-mediated immunosuppression in cholangiocarcinoma

    doi: 10.64898/2026.06.24.734341

    Figure Lengend Snippet: (A) Strategy for p16-promoter-restricted Gdf15 silencing (shRNA) and Gdf15 overexpression in orthotopic SB1 CCA. (B) Representative gross images (left) and tumor/liver weight quantification (right). (C-D) TAM and CD8 + CTL frequencies (% of CD45 + cells) in p16-shCtrl , SB-p16-shGdf15, and SB- p16-Gdf15 OE tumors via flow cytometry. (E) (A) EpCAM⁺GDF-15⁺ CCA cells (teal) adjacent to TAMs (pink); EpCAM⁺ (blue) and GDF-15⁺ (orange) transcripts shown. Scale bar 100 µm. (B) Per-TAM immunosuppressive score (per-sample z) versus distance to the nearest GDF-15⁺ or GDF-15⁻ CCA cell (TAMs ≤200 µm; n = 13,597 and 14,703 across three iCCA samples). Line/band: linear fit ± 95% CI; β and P from linear mixed-effects [score ∼ distance + (1|sample)]. The gradient is GDF-15⁺-specific (β = −3.79×10⁻³/µm, P < 10⁻¹⁰) and absent for GDF-15⁻ cells (β = +9.11×10⁻⁴/µm, P = 0.004). Scale bar, 100 µm. Data are mean ± SEM; *, P<0.05; ***, P<0.001; ns, not significant.

    Article Snippet: CD45 positive cells were enriched with CD45 (TIL) MicroBeads, mouse (Miltenyi # 130-110-618) according to the manufacturer’s instruction.

    Techniques: shRNA, Over Expression, Flow Cytometry

    Sarcoma growth and leukocyte infiltration in IL1R2-deficient mice. A–C, Tumor volume of transplantable FS6 ( A ), MN/MCA1 ( B ), and 3-MCA–induced sarcoma ( C ) in IL1R2-competent [ n = 7 ( A ), 18 ( B ), and 16 ( C )] and -deficient [ n = 7 ( A ), 19 ( B ), and 19 ( C )] mice. D, Volume and the number of lung metastasis 27 days after MN/MCA1 intramuscular injection in Il1r2 +/+ ( n = 20) and Il1r2 −/− ( n = 22) mice. E, Analysis by FACS of IL1R2 protein expression [MFI compared with fluorescence minus one (FMO)] in myeloid and lymphoid populations isolated from FS6-bearing WT mice ( n = 8–9). F and G, Frequency of IL1R2 + cells on total neutrophils ( F ) and Tregs ( G ) in healthy ( n = 6) and FS6-bearing mice ( n = 9). H and I, Analysis by FACS of myeloid population frequency on total immune cells (CD45 + ; H ) or myeloid and lymphoid cell number normalized on tumor volume (mm 3 ; I ) in FS6-bearing Il1r2 +/+ [ n = 14 ( H ) and 11 ( I )] and Il1r2 −/− [ n = 12 ( H ) and 9–10 ( I )] mice. E–I, Cell populations were defined as follows: neutrophils (Nϕ, CD11b + Ly6G + ), monocytes (Mono., CD11b + Ly6G − Ly6C + ), macrophages (Mϕ, CD11b + Ly6G − F4/80 + ), conventional CD4 + T cells (Conv. CD4 + , TCRβ + CD4 + FOXP3 − ), Tregs (TCRβ + CD4 + FOXP3 + ), CD8 + T cells (TCRβ + CD8 + ), NK cells (NK1.1 + ), and B cells (CD19 + ). J, Representative images of immunofluorescence (IF) of neutrophils (Ly6G + ) and blood vessels (CD31 + ) in FS6 tumor tissues of Il1r2 +/+ and Il1r2 −/− mice. Scale bar, 1 mm (left images) or 200 μm (right images). K, Analysis by IF of neutrophil number normalized on tissue area (mm 2 ) in FS6 tumor tissues derived from Il1r2 +/+ ( n = 8) and Il1r2 −/− ( n = 6) mice. L–O, Analysis by FACS of frequency ( L and N ) or cell number normalized on tumor volume (mm 3 ; M and O ) of neutrophils, monocytes, macrophages ( L and M ), or alveolar macrophages (CD11b − SiglecF + ; N and O ) in MN/MCA1 primary tumors ( L and M ) or metastasis ( N and O ) in Il1r2 +/+ [ n = 9 ( L and M ) and 10 ( N and O )] and Il1r2 −/− [ n = 10 ( L and M ) and 12 ( N and O )] mice. Mean ± SEM. One representative experiment of six ( A ) or two pooled experiments ( B , H , I , N , and O ); one representative experiment of two ( C , L , and M ) or four pooled experiments ( D ); and one experiment ( C , E–G , J , and K ) performed. P values determinded by two-way ANOVA ( A and B ) and two-tailed Mann–Whitney U test ( C–I and K–O ). *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001. DAPI, 4′,6-diamidino-2-phenylindole.

    Journal: Cancer Immunology Research

    Article Title: IL1R2 Deficiency Unleashes Neutrophil-Mediated Antitumor Potential in Sarcoma

    doi: 10.1158/2326-6066.CIR-25-0651

    Figure Lengend Snippet: Sarcoma growth and leukocyte infiltration in IL1R2-deficient mice. A–C, Tumor volume of transplantable FS6 ( A ), MN/MCA1 ( B ), and 3-MCA–induced sarcoma ( C ) in IL1R2-competent [ n = 7 ( A ), 18 ( B ), and 16 ( C )] and -deficient [ n = 7 ( A ), 19 ( B ), and 19 ( C )] mice. D, Volume and the number of lung metastasis 27 days after MN/MCA1 intramuscular injection in Il1r2 +/+ ( n = 20) and Il1r2 −/− ( n = 22) mice. E, Analysis by FACS of IL1R2 protein expression [MFI compared with fluorescence minus one (FMO)] in myeloid and lymphoid populations isolated from FS6-bearing WT mice ( n = 8–9). F and G, Frequency of IL1R2 + cells on total neutrophils ( F ) and Tregs ( G ) in healthy ( n = 6) and FS6-bearing mice ( n = 9). H and I, Analysis by FACS of myeloid population frequency on total immune cells (CD45 + ; H ) or myeloid and lymphoid cell number normalized on tumor volume (mm 3 ; I ) in FS6-bearing Il1r2 +/+ [ n = 14 ( H ) and 11 ( I )] and Il1r2 −/− [ n = 12 ( H ) and 9–10 ( I )] mice. E–I, Cell populations were defined as follows: neutrophils (Nϕ, CD11b + Ly6G + ), monocytes (Mono., CD11b + Ly6G − Ly6C + ), macrophages (Mϕ, CD11b + Ly6G − F4/80 + ), conventional CD4 + T cells (Conv. CD4 + , TCRβ + CD4 + FOXP3 − ), Tregs (TCRβ + CD4 + FOXP3 + ), CD8 + T cells (TCRβ + CD8 + ), NK cells (NK1.1 + ), and B cells (CD19 + ). J, Representative images of immunofluorescence (IF) of neutrophils (Ly6G + ) and blood vessels (CD31 + ) in FS6 tumor tissues of Il1r2 +/+ and Il1r2 −/− mice. Scale bar, 1 mm (left images) or 200 μm (right images). K, Analysis by IF of neutrophil number normalized on tissue area (mm 2 ) in FS6 tumor tissues derived from Il1r2 +/+ ( n = 8) and Il1r2 −/− ( n = 6) mice. L–O, Analysis by FACS of frequency ( L and N ) or cell number normalized on tumor volume (mm 3 ; M and O ) of neutrophils, monocytes, macrophages ( L and M ), or alveolar macrophages (CD11b − SiglecF + ; N and O ) in MN/MCA1 primary tumors ( L and M ) or metastasis ( N and O ) in Il1r2 +/+ [ n = 9 ( L and M ) and 10 ( N and O )] and Il1r2 −/− [ n = 10 ( L and M ) and 12 ( N and O )] mice. Mean ± SEM. One representative experiment of six ( A ) or two pooled experiments ( B , H , I , N , and O ); one representative experiment of two ( C , L , and M ) or four pooled experiments ( D ); and one experiment ( C , E–G , J , and K ) performed. P values determinded by two-way ANOVA ( A and B ) and two-tailed Mann–Whitney U test ( C–I and K–O ). *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001. DAPI, 4′,6-diamidino-2-phenylindole.

    Article Snippet: CD45 + immune cells were enriched using CD45 (TIL) MicroBeads, mouse (Miltenyi Biotec, cat. #130-110-618), following the manufacturer’s instructions.

    Techniques: Injection, Expressing, Fluorescence, Isolation, Immunofluorescence, Derivative Assay, Two Tailed Test, MANN-WHITNEY

    Enhanced emergency granulopoiesis in IL1R2-deficient sarcoma-bearing mice. A–C, Analysis by FACS of neutrophil frequency on CD45 + cells in the indicated organs 32 days ( A ) and 20 days ( B ) and in the blood over time ( C ) after FS6 injection in Il1r2 +/+ [ n = 7 ( A ), 6–7 ( B ), and 6 ( C )] and Il1r2 −/− [ n = 8 ( A ), 6–7 ( B ), and 5 ( C )] mice. D, Spleen weight and image after FS6 injection at the day of sacrifice in Il1r2 +/+ ( n = 7) and Il1r2 −/− ( n = 7) mice. E, Cell number in the BM and spleen of Il1r2 +/+ ( n = 10) and Il1r2 −/− ( n = 13) FS6-bearing mice. F, Frequencies of HSCs, progenitors, and immature (CD101 − ) or mature (CD101 + ) neutrophils on live cells in the BM and spleen of Il1r2 +/+ ( n = 5–10) and Il1r2 −/− ( n = 5–13) FS6-bearing mice. Cell populations were defined as follows: long-term HSCs (LT-HSC; Lin − c-Kit + Sca-1 + Flt3 − CD48 − CD150 + CD34 − ), MPP1 (Lin − c-Kit + Sca-1 + Flt3 − CD48 − CD150 + CD34 + ), MPP2 (Lin − c-Kit + Sca-1 + Flt3 − CD48 + CD150 + ), MPP3 (Lin − c-Kit + Sca-1 + Flt3 − CD48 + CD150 − ), MPP4 (Lin − c-Kit + Sca-1 + Flt3 + ), common myeloid progenitors (CMP; Lin − c-Kit + Sca-1 − CD34 + CD16/32 − ), GMP (Lin − c-Kit + Sca-1 − CD34 + CD16/32 + ), megakaryocyte–erythrocyte progenitors (MEP; Lin − c-Kit + Sca-1 − CD34 − CD16/32 − ), common lymphoid progenitors (CLP; Lin − Flt3 + IL7Rα + c-Kit int Sca-1 int ), proNeu1 (Lin − c-Kit + Ly6G − CD34 + CD16/32 + Flt3 − Ly6C + CD115 − CD81 + CD106 − CD11b low ), proNeu2 (Lin − c-Kit + Ly6G − CD34 + CD16/32 + Flt3 − Ly6C + CD115 − CD81 + CD106 + CD11b high ), and preNeu (Lin − CD115 − SiglecF − CD11b + Ly6G + cKit + CXCR4 + ). G, Frequency of neutrophil (Neu) subset (CD101 − or CD101 + ) on total neutrophils in the BM and spleen in Il1r2 +/+ ( n = 5) and Il1r2 −/− ( n = 5) FS6-bearing mice. H, IL1R2 expression (MFI) in the indicated BM and spleen populations of Il1r2 +/+ FS6-bearing mice ( n = 5). Mean ± SEM. One representative experiment ( A and D ), one experiment ( B and C ), two pooled experiments ( E ), and one or two pooled experiments ( F–H ) performed. P values determined by two-tailed Mann–Whitney U test ( A , B , and D–G ) or two-way ANOVA ( C ). *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001.

    Journal: Cancer Immunology Research

    Article Title: IL1R2 Deficiency Unleashes Neutrophil-Mediated Antitumor Potential in Sarcoma

    doi: 10.1158/2326-6066.CIR-25-0651

    Figure Lengend Snippet: Enhanced emergency granulopoiesis in IL1R2-deficient sarcoma-bearing mice. A–C, Analysis by FACS of neutrophil frequency on CD45 + cells in the indicated organs 32 days ( A ) and 20 days ( B ) and in the blood over time ( C ) after FS6 injection in Il1r2 +/+ [ n = 7 ( A ), 6–7 ( B ), and 6 ( C )] and Il1r2 −/− [ n = 8 ( A ), 6–7 ( B ), and 5 ( C )] mice. D, Spleen weight and image after FS6 injection at the day of sacrifice in Il1r2 +/+ ( n = 7) and Il1r2 −/− ( n = 7) mice. E, Cell number in the BM and spleen of Il1r2 +/+ ( n = 10) and Il1r2 −/− ( n = 13) FS6-bearing mice. F, Frequencies of HSCs, progenitors, and immature (CD101 − ) or mature (CD101 + ) neutrophils on live cells in the BM and spleen of Il1r2 +/+ ( n = 5–10) and Il1r2 −/− ( n = 5–13) FS6-bearing mice. Cell populations were defined as follows: long-term HSCs (LT-HSC; Lin − c-Kit + Sca-1 + Flt3 − CD48 − CD150 + CD34 − ), MPP1 (Lin − c-Kit + Sca-1 + Flt3 − CD48 − CD150 + CD34 + ), MPP2 (Lin − c-Kit + Sca-1 + Flt3 − CD48 + CD150 + ), MPP3 (Lin − c-Kit + Sca-1 + Flt3 − CD48 + CD150 − ), MPP4 (Lin − c-Kit + Sca-1 + Flt3 + ), common myeloid progenitors (CMP; Lin − c-Kit + Sca-1 − CD34 + CD16/32 − ), GMP (Lin − c-Kit + Sca-1 − CD34 + CD16/32 + ), megakaryocyte–erythrocyte progenitors (MEP; Lin − c-Kit + Sca-1 − CD34 − CD16/32 − ), common lymphoid progenitors (CLP; Lin − Flt3 + IL7Rα + c-Kit int Sca-1 int ), proNeu1 (Lin − c-Kit + Ly6G − CD34 + CD16/32 + Flt3 − Ly6C + CD115 − CD81 + CD106 − CD11b low ), proNeu2 (Lin − c-Kit + Ly6G − CD34 + CD16/32 + Flt3 − Ly6C + CD115 − CD81 + CD106 + CD11b high ), and preNeu (Lin − CD115 − SiglecF − CD11b + Ly6G + cKit + CXCR4 + ). G, Frequency of neutrophil (Neu) subset (CD101 − or CD101 + ) on total neutrophils in the BM and spleen in Il1r2 +/+ ( n = 5) and Il1r2 −/− ( n = 5) FS6-bearing mice. H, IL1R2 expression (MFI) in the indicated BM and spleen populations of Il1r2 +/+ FS6-bearing mice ( n = 5). Mean ± SEM. One representative experiment ( A and D ), one experiment ( B and C ), two pooled experiments ( E ), and one or two pooled experiments ( F–H ) performed. P values determined by two-tailed Mann–Whitney U test ( A , B , and D–G ) or two-way ANOVA ( C ). *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001.

    Article Snippet: CD45 + immune cells were enriched using CD45 (TIL) MicroBeads, mouse (Miltenyi Biotec, cat. #130-110-618), following the manufacturer’s instructions.

    Techniques: Injection, Expressing, Two Tailed Test, MANN-WHITNEY

    Cellular mechanisms of resistance to sarcoma growth in IL1R2-deficient mice. A and B, FS6 tumor growth curve (left) or primary tumor volume at the time of sacrifice (right) in Il1r2 +/+ ( n = 24), Il1r2 −/− ( n = 23), Csf3r −/− ( n = 22), and Il1r2 −/− /Csf3r −/− ( n = 19) mice ( A ) and analysis by FACS of neutrophil frequency on CD45 + cells in the spleen and tumor of sarcoma-bearing mice expressing Il1r2 +/+ ( n = 7), Il1r2 −/− ( n = 5), Csf3r −/− ( n = 6), and Il1r2 −/− /Csf3r −/− ( n = 4; B ). C–E, FS6 tumor volume ( C–E ) and growth curve ( E ) in Il1r2 +/+ and Il1r2 −/− mice treated with anti-CD8 and/or anti-NK1.1 ( C, n = 9 Il1r2 +/+ mice + ctrl IgG, n = 9 Il1r2 +/+ mice + anti-CD8, n = 8 Il1r2 −/− mice + ctrl IgG, and n = 6 Il1r2 −/− mice + anti-CD8; D, n = 8 Il1r2 +/+ mice + ctrl IgG, n = 9 Il1r2 +/+ mice + anti-NK1.1, n = 8 Il1r2 −/− mice + ctrl IgG, and n = 7 Il1r2 −/− mice + anti-NK1.1; E, n = 7 Il1r2 +/+ mice + ctrl IgG, n = 8 Il1r2 +/+ mice + anti–CD8–NK1.1, n = 6 Il1r2 −/− mice + ctrl IgG, and n = 6 Il1r2 −/− mice + anti–CD8–NK1.1). F and G, FS6 tumor growth curve in Il1r2 +/+ and Il1r2 −/− mice treated with anti–PD-1 ( F ) or anti-IFNγ ( G ; F, n = 5 Il1r2 +/+ mice + ctrl IgG, n = 6 Il1r2 +/+ mice + anti–PD-1, n = 6 Il1r2 −/− mice + ctrl IgG, and n = 7 Il1r2 −/− mice + anti–PD-1; G, n = 5 Il1r2 +/+ mice + ctrl IgG, n = 8 Il1r2 +/+ mice + anti-IFNγ, n = 7 Il1r2 −/− mice + ctrl IgG, and n = 9 Il1r2 −/− mice + anti-IFNγ). H and I, FS6 primary tumor volume in WT ( n = 16), Il1r2 −/− ( n = 5), and Il1r1 −/− ( n = 7) mice ( H ) and analysis by FACS of neutrophil frequency on CD45 + cells in the blood, spleen, and tumor of WT ( n = 10), Il1r2 −/− ( n = 5), and Il1r1 −/− ( n = 5) sarcoma-bearing mice ( I ). J, FS6 tumor growth curve in Il1r2 −/− mice treated with vehicle ( n = 9) or anakinra ( n = 11). Mean ± SEM. Three pooled experiments ( A ) and one experiment ( B–J ) performed. Experiments of panels H and I were performed using a pool of commercial and littermate WT mice that showed similar tumor growth and neutrophil frequency. P values determined by two-way ANOVA [ A and E (left), F–H , and J ] or two-tailed Mann–Whitney U test [ A and E (right), B–D , and I ]. ns, not statistically significant; *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001.

    Journal: Cancer Immunology Research

    Article Title: IL1R2 Deficiency Unleashes Neutrophil-Mediated Antitumor Potential in Sarcoma

    doi: 10.1158/2326-6066.CIR-25-0651

    Figure Lengend Snippet: Cellular mechanisms of resistance to sarcoma growth in IL1R2-deficient mice. A and B, FS6 tumor growth curve (left) or primary tumor volume at the time of sacrifice (right) in Il1r2 +/+ ( n = 24), Il1r2 −/− ( n = 23), Csf3r −/− ( n = 22), and Il1r2 −/− /Csf3r −/− ( n = 19) mice ( A ) and analysis by FACS of neutrophil frequency on CD45 + cells in the spleen and tumor of sarcoma-bearing mice expressing Il1r2 +/+ ( n = 7), Il1r2 −/− ( n = 5), Csf3r −/− ( n = 6), and Il1r2 −/− /Csf3r −/− ( n = 4; B ). C–E, FS6 tumor volume ( C–E ) and growth curve ( E ) in Il1r2 +/+ and Il1r2 −/− mice treated with anti-CD8 and/or anti-NK1.1 ( C, n = 9 Il1r2 +/+ mice + ctrl IgG, n = 9 Il1r2 +/+ mice + anti-CD8, n = 8 Il1r2 −/− mice + ctrl IgG, and n = 6 Il1r2 −/− mice + anti-CD8; D, n = 8 Il1r2 +/+ mice + ctrl IgG, n = 9 Il1r2 +/+ mice + anti-NK1.1, n = 8 Il1r2 −/− mice + ctrl IgG, and n = 7 Il1r2 −/− mice + anti-NK1.1; E, n = 7 Il1r2 +/+ mice + ctrl IgG, n = 8 Il1r2 +/+ mice + anti–CD8–NK1.1, n = 6 Il1r2 −/− mice + ctrl IgG, and n = 6 Il1r2 −/− mice + anti–CD8–NK1.1). F and G, FS6 tumor growth curve in Il1r2 +/+ and Il1r2 −/− mice treated with anti–PD-1 ( F ) or anti-IFNγ ( G ; F, n = 5 Il1r2 +/+ mice + ctrl IgG, n = 6 Il1r2 +/+ mice + anti–PD-1, n = 6 Il1r2 −/− mice + ctrl IgG, and n = 7 Il1r2 −/− mice + anti–PD-1; G, n = 5 Il1r2 +/+ mice + ctrl IgG, n = 8 Il1r2 +/+ mice + anti-IFNγ, n = 7 Il1r2 −/− mice + ctrl IgG, and n = 9 Il1r2 −/− mice + anti-IFNγ). H and I, FS6 primary tumor volume in WT ( n = 16), Il1r2 −/− ( n = 5), and Il1r1 −/− ( n = 7) mice ( H ) and analysis by FACS of neutrophil frequency on CD45 + cells in the blood, spleen, and tumor of WT ( n = 10), Il1r2 −/− ( n = 5), and Il1r1 −/− ( n = 5) sarcoma-bearing mice ( I ). J, FS6 tumor growth curve in Il1r2 −/− mice treated with vehicle ( n = 9) or anakinra ( n = 11). Mean ± SEM. Three pooled experiments ( A ) and one experiment ( B–J ) performed. Experiments of panels H and I were performed using a pool of commercial and littermate WT mice that showed similar tumor growth and neutrophil frequency. P values determined by two-way ANOVA [ A and E (left), F–H , and J ] or two-tailed Mann–Whitney U test [ A and E (right), B–D , and I ]. ns, not statistically significant; *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001.

    Article Snippet: CD45 + immune cells were enriched using CD45 (TIL) MicroBeads, mouse (Miltenyi Biotec, cat. #130-110-618), following the manufacturer’s instructions.

    Techniques: Expressing, Two Tailed Test, MANN-WHITNEY

    Phenotype of neutrophils from sarcoma-bearing IL1R2-deficient mice. A and B, Analysis by FACS of CD101 + cell frequency on total neutrophils ( A ) or frequency of CD101 + and CD101 − neutrophil subsets on total CD45 + cells in the blood, spleen, and tumor ( B ) of Il1r2 +/+ ( n = 10) and Il1r2 −/− ( n = 13) FS6-bearing mice. C–F, MFI ( C ) and frequency ( D–F ) of cells positive for selected markers on total neutrophils in the blood, spleen, and tumor of Il1r2 +/+ [ n = 5 ( C ), 10 ( D and E ), and 7 ( F )] and Il1r2 −/− [ n = 8 ( C ), 13 ( D and E ), and 5 ( F )] FS6-bearing mice. G and H, Quantification of ROS production ( G ) and frequency of iNOS + ( H ) cells gated on total neutrophils infiltrating FS6 tumors in Il1r2 +/+ [ n = 10 ( G ) and 21 ( H )] and Il1r2 −/− [ n = 14 ( G ) and 22 ( H )] mice. I and J, MFI ( I ) and frequency ( J ) of cells positive for selected markers on total neutrophils in tumors of Il1r2 +/+ ( n = 7), Il1r2 −/− ( n = 5), Csf3r −/− ( n = 6), and Il1r2 −/− /Csf3r −/− ( n = 4) FS6-bearing mice. K–M, Frequency of CD44 low/high ( K ), PD-1 + ( L ), and CD25 + ( M ) cells on tumor-infiltrating Tregs in Il1r2 +/+ [ n = 14 ( K ) and 16 ( L and M )] and Il1r2 −/− ( n = 12) FS6-bearing mice. Frequency ( N and O ) of cells positive for selected markers on Tregs in the tumor ( N ) and spleen ( O ) of Il1r2 +/+ ( n = 4) and Il1r2 −/− ( n = 5) FS6-bearing mice. Mean ± SEM. Two ( A and B , D and E , G , and K–M ) and four ( H ) pooled experiments; one representative experiment of two ( C ); and one experiment ( F , I , J , N , and O ) performed. P values determined by two-tailed Mann–Whitney U test. *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001.

    Journal: Cancer Immunology Research

    Article Title: IL1R2 Deficiency Unleashes Neutrophil-Mediated Antitumor Potential in Sarcoma

    doi: 10.1158/2326-6066.CIR-25-0651

    Figure Lengend Snippet: Phenotype of neutrophils from sarcoma-bearing IL1R2-deficient mice. A and B, Analysis by FACS of CD101 + cell frequency on total neutrophils ( A ) or frequency of CD101 + and CD101 − neutrophil subsets on total CD45 + cells in the blood, spleen, and tumor ( B ) of Il1r2 +/+ ( n = 10) and Il1r2 −/− ( n = 13) FS6-bearing mice. C–F, MFI ( C ) and frequency ( D–F ) of cells positive for selected markers on total neutrophils in the blood, spleen, and tumor of Il1r2 +/+ [ n = 5 ( C ), 10 ( D and E ), and 7 ( F )] and Il1r2 −/− [ n = 8 ( C ), 13 ( D and E ), and 5 ( F )] FS6-bearing mice. G and H, Quantification of ROS production ( G ) and frequency of iNOS + ( H ) cells gated on total neutrophils infiltrating FS6 tumors in Il1r2 +/+ [ n = 10 ( G ) and 21 ( H )] and Il1r2 −/− [ n = 14 ( G ) and 22 ( H )] mice. I and J, MFI ( I ) and frequency ( J ) of cells positive for selected markers on total neutrophils in tumors of Il1r2 +/+ ( n = 7), Il1r2 −/− ( n = 5), Csf3r −/− ( n = 6), and Il1r2 −/− /Csf3r −/− ( n = 4) FS6-bearing mice. K–M, Frequency of CD44 low/high ( K ), PD-1 + ( L ), and CD25 + ( M ) cells on tumor-infiltrating Tregs in Il1r2 +/+ [ n = 14 ( K ) and 16 ( L and M )] and Il1r2 −/− ( n = 12) FS6-bearing mice. Frequency ( N and O ) of cells positive for selected markers on Tregs in the tumor ( N ) and spleen ( O ) of Il1r2 +/+ ( n = 4) and Il1r2 −/− ( n = 5) FS6-bearing mice. Mean ± SEM. Two ( A and B , D and E , G , and K–M ) and four ( H ) pooled experiments; one representative experiment of two ( C ); and one experiment ( F , I , J , N , and O ) performed. P values determined by two-tailed Mann–Whitney U test. *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001.

    Article Snippet: CD45 + immune cells were enriched using CD45 (TIL) MicroBeads, mouse (Miltenyi Biotec, cat. #130-110-618), following the manufacturer’s instructions.

    Techniques: Two Tailed Test, MANN-WHITNEY

    a, immune cell types in the TME identified through scRNAseq of CD45 + cells isolated from orthotopically implanted M3-9-M OVA cells; b, number of immune cell types detected in M3-9-M OVA tumours through scRNAseq experiment (n = 2 pooled samples per experimental groups); c, number of significantly impacted genes obtained from pairwise comparisons (Wilcoxon rank sum test); d, circos plot of all significantly impacted genes, obtained from pairwise comparisons of all cell types measured, that overlap with each other through identical or shared pathways; e, bar graph of transcriptional regulators of 3,2-HPP impacted genes; f-m, NF-κB and IRF induction in mouse RAW-Dual™ cells and human THP1-Dual™ cells with different pathogen recognition receptor agonists in the presence of HPP metabolites (HI = heat inactivated, three combined experiments, error bars represent standard error, one-way ANOVA test).

    Journal: bioRxiv

    Article Title: Microbiome-derived hydroxyphenyl propanoates enhance antitumour immunity by potentiating gasdermin D activity in tumour-associated myeloid cells

    doi: 10.64898/2026.04.23.720410

    Figure Lengend Snippet: a, immune cell types in the TME identified through scRNAseq of CD45 + cells isolated from orthotopically implanted M3-9-M OVA cells; b, number of immune cell types detected in M3-9-M OVA tumours through scRNAseq experiment (n = 2 pooled samples per experimental groups); c, number of significantly impacted genes obtained from pairwise comparisons (Wilcoxon rank sum test); d, circos plot of all significantly impacted genes, obtained from pairwise comparisons of all cell types measured, that overlap with each other through identical or shared pathways; e, bar graph of transcriptional regulators of 3,2-HPP impacted genes; f-m, NF-κB and IRF induction in mouse RAW-Dual™ cells and human THP1-Dual™ cells with different pathogen recognition receptor agonists in the presence of HPP metabolites (HI = heat inactivated, three combined experiments, error bars represent standard error, one-way ANOVA test).

    Article Snippet: Viable cells were enriched using Dead Cell Removal Kit (130-090-101; Miltenyi Biotec), and CD45 + tumour-infiltrating immune cells were isolated using Mouse CD45 (TIL) Microbeads (130-110-618; Miltenyi Biotec).

    Techniques: Isolation