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monoclonal rat anti human cxcl16 neutralizing antibody (R&D Systems)

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R&D Systems monoclonal rat anti human cxcl16 neutralizing antibody
Monoclonal Rat Anti Human Cxcl16 Neutralizing Antibody, supplied by R&D Systems, used in various techniques. Bioz Stars score: 93/100, based on 4 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/anti+human+cxcl16+neutralizing+antibody/Human+CXCL16+Antibody/10__1158_slash_2326___6066__cir___18___0317-115-10-18
Average 93 stars, based on 4 article reviews

monoclonal rat anti human cxcl16 neutralizing antibody - by Bioz Stars, 2026-09

93/100 stars

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Recombinant:

Article Title: CXCL16 signaling mediated macrophage effects on tumor invasion of papillary thyroid carcinoma
Article Snippet: .. Reagents 72 Recombinant human CXCL16, anti-human CXCL16 neutralizing antibody, and human CXCL16 73 Quantikine ELISA Kit were purchased from R&D system (Minneapolis, MN, USA). .. TAPI-2 (a 74 metalloproteinase inhibitor) were purchased from Santa Cruz Biotechnology (Dallas, TX, USA).

Article Title: Targeting IL-17A enhances imatinib efficacy in Philadelphia chromosome-positive B-cell acute lymphoblastic leukemia
Article Snippet: The sorting strategy for Th17 cells is shown in Supplementary Fig. . B-ALL cells were isolated from patients and sorted by using MAC CD19 MicroBeads (Miltenyi Biotec, 130-050-301). .. For the coculture assay, viable Th17 cells were cocultured with B-ALL cells at a ratio of 1:1, and recombinant human CXCL16 (PeproTech, 300-55), recombinant human IL-17A (PeproTech, 200-17), the anti-human IL-17A neutralizing antibody (Bio X Cell, SIM0013), the anti-human CXCL16 neutralizing antibody (R&D, AF976), anti-goat IgG (R&D, AB-108-C) or recombinant human IgG1 Fc (Bio X Cell, BE0096) was added to the indicated coculture systems. .. The proliferation activity and apoptosis of leukemia cells were detected based on staining with the PE-conjugated anti-human CD19 antibody (BioLegend, 302254, 1:100), the APC-conjugated anti-human CD4 antibody (BioLegend, 317416, 1:100), the FITC-conjugated anti-human CD4 antibody (BioLegend, 344604, 1:100), the FITC-conjugated anti-mouse/human Ki-67 antibody (BioLegend, 151212, 1:100), or Annexin V/PI (Dojindo, AD11).

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a B220 + cells and Th17 cells in the BM niche in WT mice and BCR-ABL tTA mice ( n = 3 mice per group) were subjected to immunofluorescence staining. Representative images were shown. b The numbers of Th17 cells migrating to culture medium or to leukemia cells treated with or without 50 ng/ml rhIL-17A were determined by cell counting and FCS analysis. c Real-time PCR analysis of the relative mRNA levels of chemokine genes in SupB15 (left) and BV173 cells (right) treated with rhIL-17A (100 ng/ml) or PBS control. d The human IL-5, CXCL5, CCL5 and CXCL16 levels in the culture supernatant of SupB15 cells treated with or without rhIL-17A (100 ng/ml) were measured by ELISA. e The CXCL16 concentrations in the serum of BCR-ABL tTA mice and WT mice ( n = 5 mice per group) were quantified with a Mouse Chemokine Assay Q1 (Raybiotech). f The CXCL16 concentrations in the serum of HDs ( n = 7 samples) and primary Ph + B-ALL patients ( n = 14 samples) were measured by ELISA. g Schematic strategy for studying the differentiation of Th17 cells with or without rmCXCL16 stimulation in vitro. h Representative FACS plots and quantification of the percentage of Th17 cells in naïve CD4 + T cells with or without rmCXCL16 treatment. i Schematic strategy for studying the migration of Th17 cells cocultured with leukemia cells with or without anti-CXCL16 mAb treatment in vitro. j , k Flow cytometric analysis of the percentage of Th17 cells in the lower chambers of the inserts ( j ) and proliferation activity of leukemia cells ( k ) in a coculture system with or without anti-CXCL16 treatment. The gating strategy for isolating Th17 cells is shown in Supplementary Fig. . (b–d , h , j , k) n = 3 independent experiments. Statistical significance was calculated by ( c – f , j , k ) two-tailed Student’s t test; ( b , h ) one-way ANOVA with Tukey’s multiple comparison tests ; Data are presented as means ± S.E.M. Source data are provided as a Source Data file.

Journal: Nature Communications

Article Title: Targeting IL-17A enhances imatinib efficacy in Philadelphia chromosome-positive B-cell acute lymphoblastic leukemia

doi: 10.1038/s41467-023-44270-3

Figure Lengend Snippet: a B220 + cells and Th17 cells in the BM niche in WT mice and BCR-ABL tTA mice ( n = 3 mice per group) were subjected to immunofluorescence staining. Representative images were shown. b The numbers of Th17 cells migrating to culture medium or to leukemia cells treated with or without 50 ng/ml rhIL-17A were determined by cell counting and FCS analysis. c Real-time PCR analysis of the relative mRNA levels of chemokine genes in SupB15 (left) and BV173 cells (right) treated with rhIL-17A (100 ng/ml) or PBS control. d The human IL-5, CXCL5, CCL5 and CXCL16 levels in the culture supernatant of SupB15 cells treated with or without rhIL-17A (100 ng/ml) were measured by ELISA. e The CXCL16 concentrations in the serum of BCR-ABL tTA mice and WT mice ( n = 5 mice per group) were quantified with a Mouse Chemokine Assay Q1 (Raybiotech). f The CXCL16 concentrations in the serum of HDs ( n = 7 samples) and primary Ph + B-ALL patients ( n = 14 samples) were measured by ELISA. g Schematic strategy for studying the differentiation of Th17 cells with or without rmCXCL16 stimulation in vitro. h Representative FACS plots and quantification of the percentage of Th17 cells in naïve CD4 + T cells with or without rmCXCL16 treatment. i Schematic strategy for studying the migration of Th17 cells cocultured with leukemia cells with or without anti-CXCL16 mAb treatment in vitro. j , k Flow cytometric analysis of the percentage of Th17 cells in the lower chambers of the inserts ( j ) and proliferation activity of leukemia cells ( k ) in a coculture system with or without anti-CXCL16 treatment. The gating strategy for isolating Th17 cells is shown in Supplementary Fig. . (b–d , h , j , k) n = 3 independent experiments. Statistical significance was calculated by ( c – f , j , k ) two-tailed Student’s t test; ( b , h ) one-way ANOVA with Tukey’s multiple comparison tests ; Data are presented as means ± S.E.M. Source data are provided as a Source Data file.

Article Snippet: For the coculture assay, viable Th17 cells were cocultured with B-ALL cells at a ratio of 1:1, and recombinant human CXCL16 (PeproTech, 300-55), recombinant human IL-17A (PeproTech, 200-17), the anti-human IL-17A neutralizing antibody (Bio X Cell, SIM0013), the anti-human CXCL16 neutralizing antibody (R&D, AF976), anti-goat IgG (R&D, AB-108-C) or recombinant human IgG1 Fc (Bio X Cell, BE0096) was added to the indicated coculture systems.

Techniques: Immunofluorescence, Staining, Cell Counting, Real-time Polymerase Chain Reaction, Control, Enzyme-linked Immunosorbent Assay, In Vitro, Migration, Activity Assay, Two Tailed Test, Comparison

Primary Ph + B-ALL cells were treated with or without rhIL-17A for 24 h, and relative CXCL16 mRNA level ( a ) and CXCL16 secretion ( b ) were evaluated by real-time PCR and ELISA, respectively. c Representative immunofluorescence images of B220 (red) and CXCL16 (green) staining in spleen tissue sections of WT mice and BCR-ABL tTA mice treated with or without 50 µg/kg rmIL-17A for a duration of 3 weeks (twice a week) ( n = 3 mice per group). d Flow cytometric analysis and quantification of CXCL16 expression in primary mouse B-ALL cells treated with or without rmIL-17A. e The protein levels of p65 and p-p65 in the cytoplasm and p-p65 in the nucleus of primary mouse leukemia cells treated with or without rmIL-17A were measured by Western blotting. f Immunofluorescence of p-P65 in primary B-ALL cells treated with or without rhIL-17A. g The effect of rhIL-17A treatment on NF-kB transcriptional activity. HEK 293T cells were transfected with a synthetic NF-kB luciferase reporter construct (pNF-kB-Luc) for 12 h and then treated with different concentrations of rhIL-17A for 24 h. NF-kB transcriptional activity was detected by a luciferase assay. h ChIP‒qPCR analyses of the binding of NF-kB to the CXCL16 promoter region in SupB15 cells treated with or without rhIL-17A. i – k The effect of BAY11-7082, rIL-17A or BAY11-7082 in combination with rIL-17A on the cytoplasmic and nuclear protein levels of p65, p-p65, and CXCL16 in primary Ph + B-ALL cells. i The indicated protein band intensities were quantified using ImageJ software. The relative CXCL16 mRNA level ( j ) in primary Ph + B-ALL cells and CXCL16 protein level ( k ) in the supernatant of primary Ph + B-ALL cells were measured by RT‒PCR and ELISA, respectively. (a, b , d – k ) n = 3 independent experiments. Statistical significance was calculated by ( a , b , d ) two-tailed Student’s t-test; ( e , g – k ) one-way ANOVA with Tukey’s multiple comparison tests ; Data are presented as means ± S.E.M. Source data are provided as a Source Data file.

Journal: Nature Communications

Article Title: Targeting IL-17A enhances imatinib efficacy in Philadelphia chromosome-positive B-cell acute lymphoblastic leukemia

doi: 10.1038/s41467-023-44270-3

Figure Lengend Snippet: Primary Ph + B-ALL cells were treated with or without rhIL-17A for 24 h, and relative CXCL16 mRNA level ( a ) and CXCL16 secretion ( b ) were evaluated by real-time PCR and ELISA, respectively. c Representative immunofluorescence images of B220 (red) and CXCL16 (green) staining in spleen tissue sections of WT mice and BCR-ABL tTA mice treated with or without 50 µg/kg rmIL-17A for a duration of 3 weeks (twice a week) ( n = 3 mice per group). d Flow cytometric analysis and quantification of CXCL16 expression in primary mouse B-ALL cells treated with or without rmIL-17A. e The protein levels of p65 and p-p65 in the cytoplasm and p-p65 in the nucleus of primary mouse leukemia cells treated with or without rmIL-17A were measured by Western blotting. f Immunofluorescence of p-P65 in primary B-ALL cells treated with or without rhIL-17A. g The effect of rhIL-17A treatment on NF-kB transcriptional activity. HEK 293T cells were transfected with a synthetic NF-kB luciferase reporter construct (pNF-kB-Luc) for 12 h and then treated with different concentrations of rhIL-17A for 24 h. NF-kB transcriptional activity was detected by a luciferase assay. h ChIP‒qPCR analyses of the binding of NF-kB to the CXCL16 promoter region in SupB15 cells treated with or without rhIL-17A. i – k The effect of BAY11-7082, rIL-17A or BAY11-7082 in combination with rIL-17A on the cytoplasmic and nuclear protein levels of p65, p-p65, and CXCL16 in primary Ph + B-ALL cells. i The indicated protein band intensities were quantified using ImageJ software. The relative CXCL16 mRNA level ( j ) in primary Ph + B-ALL cells and CXCL16 protein level ( k ) in the supernatant of primary Ph + B-ALL cells were measured by RT‒PCR and ELISA, respectively. (a, b , d – k ) n = 3 independent experiments. Statistical significance was calculated by ( a , b , d ) two-tailed Student’s t-test; ( e , g – k ) one-way ANOVA with Tukey’s multiple comparison tests ; Data are presented as means ± S.E.M. Source data are provided as a Source Data file.

Techniques: Real-time Polymerase Chain Reaction, Enzyme-linked Immunosorbent Assay, Immunofluorescence, Staining, Expressing, Western Blot, Activity Assay, Transfection, Luciferase, Construct, Binding Assay, Software, Two Tailed Test, Comparison

a Flow cytometric analysis of the percentages of B220 dim CD19 + cells in BM, spleens, LNs and PB of mice with secondary transplantation treated with or without rmCXCL16 ( n = 6 mice per group). b – d Representative images of Wright-Giemsa-stained PB smears ( b , top), H&E staining of spleens ( b , bottom), spleens ( c ) and spleen weights ( d ) from the indicated mice ( n = 6 mice per group). e Representative images of Ki67 staining in the spleen tissues from the indicated mice. n = 4 fields, two different mice per group. f Flow cytometric analysis of the percentages of Th17 cells in the PB, LNs, spleens and BM from the indicated mice ( n = 6 mice per group). g Spleen tissues from the indicated mice were subjected to immunofluorescence staining for IL-17A (red), CD4 (green), and B220 (rose red). Representative images of Th17 cells were shown. n = 4 fields, two different mice per group. h Kaplan–Meier survival curves for the indicated mice ( n = 8 mice per group). i Schematic strategy for investigating the effects of anti-CXCL16 mAb alone or combined with imatinib on Ph + B-ALL progression. j – l Representative images of spleens ( j ), spleen weights ( k ), Wright-Giemsa-stained PB smears ( l, top ), and H&E staining of the spleen ( l, bottom ) from leukemia mice treated with the indicated agents ( n = 3 mice per group). m Flow cytometric analysis of the percentages of B220 dim CD19 + cells in the PB, BM, LNs and spleens from leukemia mice treated with the indicated agents ( n = 3 mice per group). n The percentage of Ki-67 + cells in the spleen was detected by immunofluorescence staining in the indicated mice. Data are presented as means ± S.E.M of eight random fields of view from three different mice per group. o Flow cytometric analysis of the percentages of Th17 cells in the PBMCs, LNs, spleens and BM of leukemia mice treated with the indicated agents ( n = 3 mice per group). (a , m ) The gating strategy for B220 dim CD19 + cells was shown in Supplementary Fig. . ( f , o ) The gating strategy for Th17 cells in the CD4 + T cells was shown in Supplementary Fig. . Statistical significance was calculated by ( a, d – g ) two-tailed Student’s t-test; ( k , m – o) one-way ANOVA with Tukey’s multiple comparison tests ; Data are presented as means ± S.E.M. Source data are provided as a Source Data file.

Journal: Nature Communications

Article Title: Targeting IL-17A enhances imatinib efficacy in Philadelphia chromosome-positive B-cell acute lymphoblastic leukemia

doi: 10.1038/s41467-023-44270-3

Figure Lengend Snippet: a Flow cytometric analysis of the percentages of B220 dim CD19 + cells in BM, spleens, LNs and PB of mice with secondary transplantation treated with or without rmCXCL16 ( n = 6 mice per group). b – d Representative images of Wright-Giemsa-stained PB smears ( b , top), H&E staining of spleens ( b , bottom), spleens ( c ) and spleen weights ( d ) from the indicated mice ( n = 6 mice per group). e Representative images of Ki67 staining in the spleen tissues from the indicated mice. n = 4 fields, two different mice per group. f Flow cytometric analysis of the percentages of Th17 cells in the PB, LNs, spleens and BM from the indicated mice ( n = 6 mice per group). g Spleen tissues from the indicated mice were subjected to immunofluorescence staining for IL-17A (red), CD4 (green), and B220 (rose red). Representative images of Th17 cells were shown. n = 4 fields, two different mice per group. h Kaplan–Meier survival curves for the indicated mice ( n = 8 mice per group). i Schematic strategy for investigating the effects of anti-CXCL16 mAb alone or combined with imatinib on Ph + B-ALL progression. j – l Representative images of spleens ( j ), spleen weights ( k ), Wright-Giemsa-stained PB smears ( l, top ), and H&E staining of the spleen ( l, bottom ) from leukemia mice treated with the indicated agents ( n = 3 mice per group). m Flow cytometric analysis of the percentages of B220 dim CD19 + cells in the PB, BM, LNs and spleens from leukemia mice treated with the indicated agents ( n = 3 mice per group). n The percentage of Ki-67 + cells in the spleen was detected by immunofluorescence staining in the indicated mice. Data are presented as means ± S.E.M of eight random fields of view from three different mice per group. o Flow cytometric analysis of the percentages of Th17 cells in the PBMCs, LNs, spleens and BM of leukemia mice treated with the indicated agents ( n = 3 mice per group). (a , m ) The gating strategy for B220 dim CD19 + cells was shown in Supplementary Fig. . ( f , o ) The gating strategy for Th17 cells in the CD4 + T cells was shown in Supplementary Fig. . Statistical significance was calculated by ( a, d – g ) two-tailed Student’s t-test; ( k , m – o) one-way ANOVA with Tukey’s multiple comparison tests ; Data are presented as means ± S.E.M. Source data are provided as a Source Data file.

Techniques: Transplantation Assay, Staining, Immunofluorescence, Two Tailed Test, Comparison

The Th17 cell population and IL-17A expression are distinctively increased in Ph + B-ALL patients, and high expression of IL-17A promotes the progression of Ph + B-ALL. IL-17A promotes the proliferation and survival of Ph + B-ALL cells by activating the BCR-ABL and IL6/JAK/STAT3 signaling pathways. Moreover, IL-17A can increase the secretion of the chemokine CXCL16 from leukemia cells by activating NF-kB, which in turn mediates the differentiation and recruitment of Th17 cells to the leukemia niche microenvironment. Targeting IL-17A or CXCL16 in the leukemia niche microenvironment attenuates the progression of Ph + B-ALL.

Journal: Nature Communications

Article Title: Targeting IL-17A enhances imatinib efficacy in Philadelphia chromosome-positive B-cell acute lymphoblastic leukemia

doi: 10.1038/s41467-023-44270-3

Figure Lengend Snippet: The Th17 cell population and IL-17A expression are distinctively increased in Ph + B-ALL patients, and high expression of IL-17A promotes the progression of Ph + B-ALL. IL-17A promotes the proliferation and survival of Ph + B-ALL cells by activating the BCR-ABL and IL6/JAK/STAT3 signaling pathways. Moreover, IL-17A can increase the secretion of the chemokine CXCL16 from leukemia cells by activating NF-kB, which in turn mediates the differentiation and recruitment of Th17 cells to the leukemia niche microenvironment. Targeting IL-17A or CXCL16 in the leukemia niche microenvironment attenuates the progression of Ph + B-ALL.

Techniques: Expressing, Protein-Protein interactions

Figure 2. Enhanced CXCL16 expressions in PTC tumor microenvironment. (A) CXCL16 levels were measured

Journal: Endocrine-related cancer

Article Title: CXCL16 signaling mediated macrophage effects on tumor invasion of papillary thyroid carcinoma.

doi: 10.1530/ERC-15-0196

Figure Lengend Snippet: Figure 2. Enhanced CXCL16 expressions in PTC tumor microenvironment. (A) CXCL16 levels were measured

Article Snippet: Reagents 72 Recombinant human CXCL16, anti-human CXCL16 neutralizing antibody, and human CXCL16 73 Quantikine ELISA Kit were purchased from R&D system (Minneapolis, MN, USA).

Techniques:

Figure 4. CXCL16 mediated macrophage polarization in PTC tumor microenvironments. (A) Primary monocytes were treated with 50% CMs from H tori, BHP10-3, and KTC-1. CMs of BHP10-3 and KTC-1 groups were treated with anti-CXCL16 antibodies (100 ug/ml), simultaneously. mRNA expressions of CD163,

Journal: Endocrine-related cancer

Article Title: CXCL16 signaling mediated macrophage effects on tumor invasion of papillary thyroid carcinoma.

doi: 10.1530/ERC-15-0196

Figure Lengend Snippet: Figure 4. CXCL16 mediated macrophage polarization in PTC tumor microenvironments. (A) Primary monocytes were treated with 50% CMs from H tori, BHP10-3, and KTC-1. CMs of BHP10-3 and KTC-1 groups were treated with anti-CXCL16 antibodies (100 ug/ml), simultaneously. mRNA expressions of CD163,

Article Snippet: Reagents 72 Recombinant human CXCL16, anti-human CXCL16 neutralizing antibody, and human CXCL16 73 Quantikine ELISA Kit were purchased from R&D system (Minneapolis, MN, USA).

Techniques:

Figure 5. Expression of CXCR6 or CXCL16 in PTC tissues. Immunohistochemical staining was done in the PTC tissue microarray with anti-CXCR6 or anti-CXCL16 antibodies (n=143). Representative images of (A) cancer-

Journal: Endocrine-related cancer

Article Title: CXCL16 signaling mediated macrophage effects on tumor invasion of papillary thyroid carcinoma.

doi: 10.1530/ERC-15-0196

Figure Lengend Snippet: Figure 5. Expression of CXCR6 or CXCL16 in PTC tissues. Immunohistochemical staining was done in the PTC tissue microarray with anti-CXCR6 or anti-CXCL16 antibodies (n=143). Representative images of (A) cancer-

Article Snippet: Reagents 72 Recombinant human CXCL16, anti-human CXCL16 neutralizing antibody, and human CXCL16 73 Quantikine ELISA Kit were purchased from R&D system (Minneapolis, MN, USA).

Techniques: Expressing, Immunohistochemical staining, Staining, Microarray

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monoclonal rat anti human cxcl16 neutralizing antibody (R&D Systems)

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