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anti cxcr3 neutralizing antibody  (Bio X Cell)


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    Structured Review

    Bio X Cell anti cxcr3 neutralizing antibody
    Anti Cxcr3 Neutralizing Antibody, supplied by Bio X Cell, used in various techniques. Bioz Stars score: 95/100, based on 110 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/anti+cxcr3+neutralizing+antibody/pm41776161-229-60-66?v=Bio+X+Cell
    Average 95 stars, based on 110 article reviews
    anti cxcr3 neutralizing antibody - by Bioz Stars, 2026-07
    95/100 stars

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    CXCL10 is a critical factor in KRAS-mutated lung cancer treated with MEKi+RT. (A) Tissue sequencing reveals enrichment of the chemokine signaling pathway. (B-D) Sequencing data indicate CXCL10, <t>CXCR3,</t> and STING expression across four groups. (E) CXCL10 mRNA and protein levels in A549 post-MEKi and RT treatment. (F) CXCL10 mRNA and protein levels in H23 post-MEKi and RT treatment. (G) Mice injected with LLC cells were categorized into control, MEKi+ RT+anti-CXCR3, and MEKi+RT+isotype groups, with the tumor sizes measured. (H) Tumor growth curves for the three groups. (I) Tumor weight comparison post-excision. (J-L) Flow cytometry comparison of CD3+, CD8+, and CD4+ T lymphocyte counts in tumors. (M) Flow cytometry plots showing CD3+ T cell gating in the three groups. * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.0001. CXCL, C-X-C motif chemokine ligand; CXCR, C-X-C motif chemokine receptor; MEKi, MEK inhibitor; RT, radiotherapy; STING, stimulator of interferon genes.
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    CXCL10 is a critical factor in KRAS-mutated lung cancer treated with MEKi+RT. (A) Tissue sequencing reveals enrichment of the chemokine signaling pathway. (B-D) Sequencing data indicate CXCL10, CXCR3, and STING expression across four groups. (E) CXCL10 mRNA and protein levels in A549 post-MEKi and RT treatment. (F) CXCL10 mRNA and protein levels in H23 post-MEKi and RT treatment. (G) Mice injected with LLC cells were categorized into control, MEKi+ RT+anti-CXCR3, and MEKi+RT+isotype groups, with the tumor sizes measured. (H) Tumor growth curves for the three groups. (I) Tumor weight comparison post-excision. (J-L) Flow cytometry comparison of CD3+, CD8+, and CD4+ T lymphocyte counts in tumors. (M) Flow cytometry plots showing CD3+ T cell gating in the three groups. * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.0001. CXCL, C-X-C motif chemokine ligand; CXCR, C-X-C motif chemokine receptor; MEKi, MEK inhibitor; RT, radiotherapy; STING, stimulator of interferon genes.

    Journal: Frontiers in Immunology

    Article Title: Impact of MEK inhibition on T-cell infiltration and function after radiotherapy in KRAS-mutant lung cancer

    doi: 10.3389/fimmu.2025.1663502

    Figure Lengend Snippet: CXCL10 is a critical factor in KRAS-mutated lung cancer treated with MEKi+RT. (A) Tissue sequencing reveals enrichment of the chemokine signaling pathway. (B-D) Sequencing data indicate CXCL10, CXCR3, and STING expression across four groups. (E) CXCL10 mRNA and protein levels in A549 post-MEKi and RT treatment. (F) CXCL10 mRNA and protein levels in H23 post-MEKi and RT treatment. (G) Mice injected with LLC cells were categorized into control, MEKi+ RT+anti-CXCR3, and MEKi+RT+isotype groups, with the tumor sizes measured. (H) Tumor growth curves for the three groups. (I) Tumor weight comparison post-excision. (J-L) Flow cytometry comparison of CD3+, CD8+, and CD4+ T lymphocyte counts in tumors. (M) Flow cytometry plots showing CD3+ T cell gating in the three groups. * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.0001. CXCL, C-X-C motif chemokine ligand; CXCR, C-X-C motif chemokine receptor; MEKi, MEK inhibitor; RT, radiotherapy; STING, stimulator of interferon genes.

    Article Snippet: After 2 days of oral gavage, the mice in the combined therapy groups received radiation (8 Gy/1F), and 200 μg of CXCR3 neutralizing antibody (Bioxcell, Cat. No. BE0249) or the isotype (Bioxcell, Cat. No. BE0091) was injected intraperitoneally twice a week.

    Techniques: Sequencing, Expressing, Injection, Control, Comparison, Flow Cytometry

    Neutralization of chemokine receptor CXCR3 and co-culture experiments with CD8 + T cells and Huh7 cells. ( A ) Schematic of the treatment used in the DEN-induced HCC mouse models. ( B ) Liver tumors in the DEN-induced HCC mouse models treated as shown in panel A (n = 4 for each group). Yellow arrows indicate liver tumors. ∗ P < .05, ∗∗ P < .01. ( C ) Immunostaining for CD3-positive cells in the liver tumors of the DEN-induced HCC mouse models in groups, as shown in panel A (n = 3 for each group) (original magnification: ×400). Black arrows indicate CD3-positive T cells. Positively stained cells were quantified as described in <xref ref-type=Figure 4 G . ∗ P < .05, ∗∗∗ P < .001. ( D ) Schematic of the experiments of human CD8 + T cells co-cultured with Huh7 cells treated with 2DG-PLGA-NPs or PLGA. ( E ) Lactate levels in the supernatant of the Huh7 cell culture treated with 2DG-PLGA-NPs (equivalent to 10 mmol/L 2DG) or PLGA (same weight as 2DG-PLGA) for 24 hours in the absence or presence of glucose (900 mg/dL). ∗∗∗ P < .001. ( F ) IFN -γ mRNA levels in the CD8 + T cells co-cultured with the Huh7 cells treated with 2DG-PLGA-NPs or PLGA for 4 hours in the absence or presence of glucose (900 mg/dL). ∗ P < .05, ∗∗ P < .01, and ∗∗∗ P < .001. 2-NBDG uptake in the ( G ) Huh7 cells and ( H ) CD8 + T cells after CD8 + T cells were co-cultured with Huh7 cells treated with 2DG-PLGA-NPs or PLGA for 16 hours in the absence or presence of glucose (900 mg/dL). ∗ P < .05, ∗∗ P < .01, and ∗∗∗ P < .001. i.p., intraperitoneal injection; i.v., intravenous injection. " width="100%" height="100%">

    Journal: Cellular and Molecular Gastroenterology and Hepatology

    Article Title: Nanoparticle-Mediated Delivery of 2-Deoxy-D-Glucose Induces Antitumor Immunity and Cytotoxicity in Liver Tumors in Mice

    doi: 10.1016/j.jcmgh.2020.10.010

    Figure Lengend Snippet: Neutralization of chemokine receptor CXCR3 and co-culture experiments with CD8 + T cells and Huh7 cells. ( A ) Schematic of the treatment used in the DEN-induced HCC mouse models. ( B ) Liver tumors in the DEN-induced HCC mouse models treated as shown in panel A (n = 4 for each group). Yellow arrows indicate liver tumors. ∗ P < .05, ∗∗ P < .01. ( C ) Immunostaining for CD3-positive cells in the liver tumors of the DEN-induced HCC mouse models in groups, as shown in panel A (n = 3 for each group) (original magnification: ×400). Black arrows indicate CD3-positive T cells. Positively stained cells were quantified as described in Figure 4 G . ∗ P < .05, ∗∗∗ P < .001. ( D ) Schematic of the experiments of human CD8 + T cells co-cultured with Huh7 cells treated with 2DG-PLGA-NPs or PLGA. ( E ) Lactate levels in the supernatant of the Huh7 cell culture treated with 2DG-PLGA-NPs (equivalent to 10 mmol/L 2DG) or PLGA (same weight as 2DG-PLGA) for 24 hours in the absence or presence of glucose (900 mg/dL). ∗∗∗ P < .001. ( F ) IFN -γ mRNA levels in the CD8 + T cells co-cultured with the Huh7 cells treated with 2DG-PLGA-NPs or PLGA for 4 hours in the absence or presence of glucose (900 mg/dL). ∗ P < .05, ∗∗ P < .01, and ∗∗∗ P < .001. 2-NBDG uptake in the ( G ) Huh7 cells and ( H ) CD8 + T cells after CD8 + T cells were co-cultured with Huh7 cells treated with 2DG-PLGA-NPs or PLGA for 16 hours in the absence or presence of glucose (900 mg/dL). ∗ P < .05, ∗∗ P < .01, and ∗∗∗ P < .001. i.p., intraperitoneal injection; i.v., intravenous injection.

    Article Snippet: The culture supernatant was injected into the chemoattractant injection side of the microchannel with or without an anti-CXCR3 neutralizing antibody (Bio X Cell).

    Techniques: Neutralization, Co-Culture Assay, Immunostaining, Staining, Cell Culture, Injection

    CD8 + T-cell and Treg migration in 260-μm–long microchannels. ( A ) After aligning the CD8 + T cells (5 × 10 4 cells/well) on the edge of a microchannel ( bottom of each panel ), medium containing CXCL10 and glucose ( lane 1 ); CXCL10, glucose, and lactate ( lane 2 ); or CXCL10, glucose, and hydrochloric acid ( lane 3 ) were injected into the compartment opposite site the CD8 + T-cell–containing compartment. CD8 + T cells in the images ( middle line of each panel ) are represented by red dots in each panel in the third line. Migration of the CD8 + T cells randomly selected from those in each lane was analyzed using TAXIScan Analyzer 2 software. To obtain statistical data of cell migration, median values of velocity and directionality (direction toward ligands) for each cell within an experimental period were calculated from the migratory pathway data obtained from time-lapse images. Data are expressed in velocity-directionality plots. ∗ P < .05, ∗∗ P < .01, and ∗∗∗ P < .001. ( B ) Migration of the CD8 + T cells co-cultured with IFN-γ (1 μg/mL) for 20 hours was analyzed in the same manner as described in panel A except for the injected medium ( lane 1 , none; lane 2 , culture supernatant of the CD8 + T cells with IFN-γ; lane 3 , culture supernatant of the CD8 + T cells with IFN-γ + anti-CXCR3). ∗∗∗ P < .001. ( C ) mRNA levels of CXCL9 / CXCL10 / CXCL11 in the CD8 + T cells co-cultured with or without IFN-γ. ∗ P < .05, ∗∗ P < .01. ( D ) Huh7 cells (1 × 10 4 cells/well) that were incubated with or without 2DG (10 mmol/L) for 24 hours, with or without the addition of IFN-γ and TNF-α for the final 12 hours of the experiment, were added into the chemoattractant injection side of the microchannel. CD8 + T-cell migration was analyzed in the same manner as described for panel A , except the injected medium was added to the compartment opposite the CD8+ T-cell–containing compartment ( lane 1, none; lane 2 , none; lane 3 , none; and lane 4 , anti-CXCR3). CD8 + T cells in the images were generated in the same manner as described in panel A . ∗ P < .05, ∗∗∗ P < .001. ( E ) After aligning the CD8 + T cells (5 × 10 4 cells/well) on the edge of the microchannel ( bottom in each panel ), medium containing CXCL10 ( lane 1 ); CXCL10 and glucose ( lane 2 ); CXCL10, glucose, and 1 mmol/L 2DG ( lane 3 ); or CXCL10, glucose, and 10 mmol/L 2DG ( lane 4 ) was injected into the compartment on the opposite side of the CD8 + T-cell–containing compartment. The CD8 + T cells in the images were drawn in the same manner as described in panel A . ∗ P < .05, ∗∗ P < .01, and ∗∗∗ P < .001.

    Journal: Cellular and Molecular Gastroenterology and Hepatology

    Article Title: Nanoparticle-Mediated Delivery of 2-Deoxy-D-Glucose Induces Antitumor Immunity and Cytotoxicity in Liver Tumors in Mice

    doi: 10.1016/j.jcmgh.2020.10.010

    Figure Lengend Snippet: CD8 + T-cell and Treg migration in 260-μm–long microchannels. ( A ) After aligning the CD8 + T cells (5 × 10 4 cells/well) on the edge of a microchannel ( bottom of each panel ), medium containing CXCL10 and glucose ( lane 1 ); CXCL10, glucose, and lactate ( lane 2 ); or CXCL10, glucose, and hydrochloric acid ( lane 3 ) were injected into the compartment opposite site the CD8 + T-cell–containing compartment. CD8 + T cells in the images ( middle line of each panel ) are represented by red dots in each panel in the third line. Migration of the CD8 + T cells randomly selected from those in each lane was analyzed using TAXIScan Analyzer 2 software. To obtain statistical data of cell migration, median values of velocity and directionality (direction toward ligands) for each cell within an experimental period were calculated from the migratory pathway data obtained from time-lapse images. Data are expressed in velocity-directionality plots. ∗ P < .05, ∗∗ P < .01, and ∗∗∗ P < .001. ( B ) Migration of the CD8 + T cells co-cultured with IFN-γ (1 μg/mL) for 20 hours was analyzed in the same manner as described in panel A except for the injected medium ( lane 1 , none; lane 2 , culture supernatant of the CD8 + T cells with IFN-γ; lane 3 , culture supernatant of the CD8 + T cells with IFN-γ + anti-CXCR3). ∗∗∗ P < .001. ( C ) mRNA levels of CXCL9 / CXCL10 / CXCL11 in the CD8 + T cells co-cultured with or without IFN-γ. ∗ P < .05, ∗∗ P < .01. ( D ) Huh7 cells (1 × 10 4 cells/well) that were incubated with or without 2DG (10 mmol/L) for 24 hours, with or without the addition of IFN-γ and TNF-α for the final 12 hours of the experiment, were added into the chemoattractant injection side of the microchannel. CD8 + T-cell migration was analyzed in the same manner as described for panel A , except the injected medium was added to the compartment opposite the CD8+ T-cell–containing compartment ( lane 1, none; lane 2 , none; lane 3 , none; and lane 4 , anti-CXCR3). CD8 + T cells in the images were generated in the same manner as described in panel A . ∗ P < .05, ∗∗∗ P < .001. ( E ) After aligning the CD8 + T cells (5 × 10 4 cells/well) on the edge of the microchannel ( bottom in each panel ), medium containing CXCL10 ( lane 1 ); CXCL10 and glucose ( lane 2 ); CXCL10, glucose, and 1 mmol/L 2DG ( lane 3 ); or CXCL10, glucose, and 10 mmol/L 2DG ( lane 4 ) was injected into the compartment on the opposite side of the CD8 + T-cell–containing compartment. The CD8 + T cells in the images were drawn in the same manner as described in panel A . ∗ P < .05, ∗∗ P < .01, and ∗∗∗ P < .001.

    Article Snippet: The culture supernatant was injected into the chemoattractant injection side of the microchannel with or without an anti-CXCR3 neutralizing antibody (Bio X Cell).

    Techniques: Migration, Injection, Software, Cell Culture, Incubation, Generated

    Neutralization of chemokine receptor CXCR3 and amplification of the antitumor effects of sorafenib by 2DG-PLGA-NPs. ( A ) Schematic of the treatment of syngeneic mice transplanted with B16F10 cells. ( B ) Tumors and growth curves of the syngeneic mice treated as shown in panel A (n = 5 for each group). ∗ P < .05 vs c; ∗∗ P < .01 vs a, b, and d; # P < .05 vs a and b. ( C ) Immunostaining for CD3-positive T cells in the tumors of the syngeneic mice treated as shown in panel A (n = 3 for each group) (original magnification: ×400). Black arrows indicate CD3-positive T cells. Positively stained cells were quantified as described in <xref ref-type=Figure 4 G . ∗∗ P < .01. ( D ) Huh7 cell xenograft tumors and growth curves of the mice 21 days after treatment was initiated in 7 groups. Mice without treatment (control) (a), mice with intravenous administration of PLGA (800 mg/kg) weekly for 3 weeks (b), mice with intraperitoneal administration of 2DG (1000 mg/kg) daily for 3 weeks (c), mice with intravenous administration of 2DG-PLGA-NPs (800 mg/kg) weekly for 3 weeks (d), mice with intravenous administration of PLGA (800 mg/kg) weekly and administration of sorafenib [5 mg/kg] daily by gastric intubation for 3 weeks (e), mice with intraperitoneal administration of 2DG (1000 mg/kg) daily and administration of sorafenib (5 mg/kg) daily by gastric intubation for 3 weeks (f), and mice with intravenous administration of 2DG-PLGA-NPs (800 mg/kg) weekly and administration of sorafenib (5 mg/kg) daily by gastric intubation for 3 weeks (g). # P < .01 vs a, b, and e; ∗ P < .05 vs. b, ∗∗ P < .01 vs a; ‡ P < .001 vs a and b; §§ P < .01 vs a, b, and e, and § P < .01 vs c. ( E ) Changes in body weight, diet consumption, liver weight, and biological markers in plasma in the same groups as indicated in panel D . ∗ P < .05, ∗∗∗ P < .001. " width="100%" height="100%">

    Journal: Cellular and Molecular Gastroenterology and Hepatology

    Article Title: Nanoparticle-Mediated Delivery of 2-Deoxy-D-Glucose Induces Antitumor Immunity and Cytotoxicity in Liver Tumors in Mice

    doi: 10.1016/j.jcmgh.2020.10.010

    Figure Lengend Snippet: Neutralization of chemokine receptor CXCR3 and amplification of the antitumor effects of sorafenib by 2DG-PLGA-NPs. ( A ) Schematic of the treatment of syngeneic mice transplanted with B16F10 cells. ( B ) Tumors and growth curves of the syngeneic mice treated as shown in panel A (n = 5 for each group). ∗ P < .05 vs c; ∗∗ P < .01 vs a, b, and d; # P < .05 vs a and b. ( C ) Immunostaining for CD3-positive T cells in the tumors of the syngeneic mice treated as shown in panel A (n = 3 for each group) (original magnification: ×400). Black arrows indicate CD3-positive T cells. Positively stained cells were quantified as described in Figure 4 G . ∗∗ P < .01. ( D ) Huh7 cell xenograft tumors and growth curves of the mice 21 days after treatment was initiated in 7 groups. Mice without treatment (control) (a), mice with intravenous administration of PLGA (800 mg/kg) weekly for 3 weeks (b), mice with intraperitoneal administration of 2DG (1000 mg/kg) daily for 3 weeks (c), mice with intravenous administration of 2DG-PLGA-NPs (800 mg/kg) weekly for 3 weeks (d), mice with intravenous administration of PLGA (800 mg/kg) weekly and administration of sorafenib [5 mg/kg] daily by gastric intubation for 3 weeks (e), mice with intraperitoneal administration of 2DG (1000 mg/kg) daily and administration of sorafenib (5 mg/kg) daily by gastric intubation for 3 weeks (f), and mice with intravenous administration of 2DG-PLGA-NPs (800 mg/kg) weekly and administration of sorafenib (5 mg/kg) daily by gastric intubation for 3 weeks (g). # P < .01 vs a, b, and e; ∗ P < .05 vs. b, ∗∗ P < .01 vs a; ‡ P < .001 vs a and b; §§ P < .01 vs a, b, and e, and § P < .01 vs c. ( E ) Changes in body weight, diet consumption, liver weight, and biological markers in plasma in the same groups as indicated in panel D . ∗ P < .05, ∗∗∗ P < .001.

    Article Snippet: The culture supernatant was injected into the chemoattractant injection side of the microchannel with or without an anti-CXCR3 neutralizing antibody (Bio X Cell).

    Techniques: Neutralization, Amplification, Immunostaining, Staining, Control, Clinical Proteomics