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PeproTech human cxcl11 elisa kit
SP-A attenuates antiviral gene expression and chemokine secretion induced by RV-C15. Differentiated NECs were challenged with RV-C15-GFP as described in . mRNA expression of MDA5 , IRF7 , IFNλ , and <t>CXCL11</t> were quantified by RT-qPCR by using RNA of NECs from non-asthmatics ( n = 6) ( a ) and asthmatics ( n = 10) ( b ). Data are shown as means ± SD from duplicated well in each condition for each donor. Secretion of CXCL11 in apical media was quantified by ELISA in ( c ). The data are means ± SD using cells from 5 non-asthmatic and 6 asthmatic donors; experiments limited by cell availability. p -values were shown in comparison to the condition of RV-C15 48 h alone.
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1) Product Images from "Surfactant Protein A Inhibits Human Rhinovirus C Binding and Infection of Airway Epithelial Cells from Pediatric Asthma"

Article Title: Surfactant Protein A Inhibits Human Rhinovirus C Binding and Infection of Airway Epithelial Cells from Pediatric Asthma

Journal: Viruses

doi: 10.3390/v16111709

SP-A attenuates antiviral gene expression and chemokine secretion induced by RV-C15. Differentiated NECs were challenged with RV-C15-GFP as described in . mRNA expression of MDA5 , IRF7 , IFNλ , and CXCL11 were quantified by RT-qPCR by using RNA of NECs from non-asthmatics ( n = 6) ( a ) and asthmatics ( n = 10) ( b ). Data are shown as means ± SD from duplicated well in each condition for each donor. Secretion of CXCL11 in apical media was quantified by ELISA in ( c ). The data are means ± SD using cells from 5 non-asthmatic and 6 asthmatic donors; experiments limited by cell availability. p -values were shown in comparison to the condition of RV-C15 48 h alone.
Figure Legend Snippet: SP-A attenuates antiviral gene expression and chemokine secretion induced by RV-C15. Differentiated NECs were challenged with RV-C15-GFP as described in . mRNA expression of MDA5 , IRF7 , IFNλ , and CXCL11 were quantified by RT-qPCR by using RNA of NECs from non-asthmatics ( n = 6) ( a ) and asthmatics ( n = 10) ( b ). Data are shown as means ± SD from duplicated well in each condition for each donor. Secretion of CXCL11 in apical media was quantified by ELISA in ( c ). The data are means ± SD using cells from 5 non-asthmatic and 6 asthmatic donors; experiments limited by cell availability. p -values were shown in comparison to the condition of RV-C15 48 h alone.

Techniques Used: Expressing, Quantitative RT-PCR, Enzyme-linked Immunosorbent Assay, Comparison



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Plac1 + tumor cells shape the immunosuppressive TME through recruiting CD4 + T cells and promoting Treg differentiation. A) Lollipop plot shows correlation of different immune cells with Plac1 expression in the TCGA‐HNSC cohort. B) Comparison of cell–cell interaction strengths of Plac1 + and Plac1 − malignant epithelial cells with other immune cells. C,D) Pearson correlation of Plac1 + cell count with Treg count in HNSCC tumor tissues. Representative mIF images of Plac1‐low and ‐high samples are shown in (D) (n = 51). Dapi (blue), Plac1 (green), CD4 (red), Foxp3 (grey), in individual and merged channels are shown. Scale bar, 200 µm and 50 µm. E) Bubble plot shows the interaction pairs between Plac1 + and Plac1 − malignant epithelial cells and CD4 T subpopulations. F) Quantification of <t>CXCL11</t> concentration in supernatant of Plac1‐NC, Plac1‐KO, Plac1‐VEC, and Plac1‐OE HNSCC cells (n = 3). G) Quantification of migrated CD4 + T cells after cocultured with HNSCC cells of different groups (n = 3). H) Representative mIF images show cell–cell interaction of malignant epithelial cells and CD4 + T cells with PVR‐TIGIT pairs. Green: CK5, red: PVR, purple: CD4, grey: TIGIT, blue: Dapi. Scale bar = 50 µm. (I) Representative GO (up) and KEGG pathways (down) enrichment of the predicted target genes expressed in CD4 + T cells by Nichenet algorithm. J,K) Representative flow cytometry images (J) and quantification results (K) of Treg ratio of CD4 + T cells after coculture with Plac1‐NC/KD (up) and Plac1‐VEC/OE (down) HNSCC cells with different treatments (n = 3). P values were calculated by two‐sided Student's t ‐test in F, G, K, by empirical shuffling in E, and by hypergeometric test in I. * p < 0.05, ** p < 0.01, *** p < 0.001.
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Plac1 + tumor cells shape the immunosuppressive TME through recruiting CD4 + T cells and promoting Treg differentiation. A) Lollipop plot shows correlation of different immune cells with Plac1 expression in the TCGA‐HNSC cohort. B) Comparison of cell–cell interaction strengths of Plac1 + and Plac1 − malignant epithelial cells with other immune cells. C,D) Pearson correlation of Plac1 + cell count with Treg count in HNSCC tumor tissues. Representative mIF images of Plac1‐low and ‐high samples are shown in (D) (n = 51). Dapi (blue), Plac1 (green), CD4 (red), Foxp3 (grey), in individual and merged channels are shown. Scale bar, 200 µm and 50 µm. E) Bubble plot shows the interaction pairs between Plac1 + and Plac1 − malignant epithelial cells and CD4 T subpopulations. F) Quantification of <t>CXCL11</t> concentration in supernatant of Plac1‐NC, Plac1‐KO, Plac1‐VEC, and Plac1‐OE HNSCC cells (n = 3). G) Quantification of migrated CD4 + T cells after cocultured with HNSCC cells of different groups (n = 3). H) Representative mIF images show cell–cell interaction of malignant epithelial cells and CD4 + T cells with PVR‐TIGIT pairs. Green: CK5, red: PVR, purple: CD4, grey: TIGIT, blue: Dapi. Scale bar = 50 µm. (I) Representative GO (up) and KEGG pathways (down) enrichment of the predicted target genes expressed in CD4 + T cells by Nichenet algorithm. J,K) Representative flow cytometry images (J) and quantification results (K) of Treg ratio of CD4 + T cells after coculture with Plac1‐NC/KD (up) and Plac1‐VEC/OE (down) HNSCC cells with different treatments (n = 3). P values were calculated by two‐sided Student's t ‐test in F, G, K, by empirical shuffling in E, and by hypergeometric test in I. * p < 0.05, ** p < 0.01, *** p < 0.001.
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Fig. 7. FABP5 downregulation in DSCs repressed <t>CXCL11/CXCR3</t> signaling between DSCs and HTR-8/Svneo cells. (A) KEGG pathway analysis of DEGs identified by RNA-seq in FABP5-knockdown primary DSC. (B) Gene Set Enrichment Analysis (GSEA) of chemokine signaling pathways in FABP5-silenced DSCs. (C) FPKM values of CXCL11 expression in control and FABP5-knockdown groups. (D) RT-qPCR, (E, F) Western blot, and (G) ELISA quantification of CXCL11 expression in DSCs transfected with FABP5-targeting or NC siRNAs. (H) RT-qPCR and (I, J) Western blot analyses of CXCR3 expression in HTR-8/Svneo cells treated with CS from FABP5-deficient or control DSCs. Statistical significance: *P < 0.05, **P < 0.01.
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Fig. 7. FABP5 downregulation in DSCs repressed <t>CXCL11/CXCR3</t> signaling between DSCs and HTR-8/Svneo cells. (A) KEGG pathway analysis of DEGs identified by RNA-seq in FABP5-knockdown primary DSC. (B) Gene Set Enrichment Analysis (GSEA) of chemokine signaling pathways in FABP5-silenced DSCs. (C) FPKM values of CXCL11 expression in control and FABP5-knockdown groups. (D) RT-qPCR, (E, F) Western blot, and (G) ELISA quantification of CXCL11 expression in DSCs transfected with FABP5-targeting or NC siRNAs. (H) RT-qPCR and (I, J) Western blot analyses of CXCR3 expression in HTR-8/Svneo cells treated with CS from FABP5-deficient or control DSCs. Statistical significance: *P < 0.05, **P < 0.01.
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SP-A attenuates antiviral gene expression and chemokine secretion induced by RV-C15. Differentiated NECs were challenged with RV-C15-GFP as described in . mRNA expression of MDA5 , IRF7 , IFNλ , and <t>CXCL11</t> were quantified by RT-qPCR by using RNA of NECs from non-asthmatics ( n = 6) ( a ) and asthmatics ( n = 10) ( b ). Data are shown as means ± SD from duplicated well in each condition for each donor. Secretion of CXCL11 in apical media was quantified by ELISA in ( c ). The data are means ± SD using cells from 5 non-asthmatic and 6 asthmatic donors; experiments limited by cell availability. p -values were shown in comparison to the condition of RV-C15 48 h alone.
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SP-A attenuates antiviral gene expression and chemokine secretion induced by RV-C15. Differentiated NECs were challenged with RV-C15-GFP as described in . mRNA expression of MDA5 , IRF7 , IFNλ , and <t>CXCL11</t> were quantified by RT-qPCR by using RNA of NECs from non-asthmatics ( n = 6) ( a ) and asthmatics ( n = 10) ( b ). Data are shown as means ± SD from duplicated well in each condition for each donor. Secretion of CXCL11 in apical media was quantified by ELISA in ( c ). The data are means ± SD using cells from 5 non-asthmatic and 6 asthmatic donors; experiments limited by cell availability. p -values were shown in comparison to the condition of RV-C15 48 h alone.
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SP-A attenuates antiviral gene expression and chemokine secretion induced by RV-C15. Differentiated NECs were challenged with RV-C15-GFP as described in . mRNA expression of MDA5 , IRF7 , IFNλ , and <t>CXCL11</t> were quantified by RT-qPCR by using RNA of NECs from non-asthmatics ( n = 6) ( a ) and asthmatics ( n = 10) ( b ). Data are shown as means ± SD from duplicated well in each condition for each donor. Secretion of CXCL11 in apical media was quantified by ELISA in ( c ). The data are means ± SD using cells from 5 non-asthmatic and 6 asthmatic donors; experiments limited by cell availability. p -values were shown in comparison to the condition of RV-C15 48 h alone.
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Image Search Results


Plac1 + tumor cells shape the immunosuppressive TME through recruiting CD4 + T cells and promoting Treg differentiation. A) Lollipop plot shows correlation of different immune cells with Plac1 expression in the TCGA‐HNSC cohort. B) Comparison of cell–cell interaction strengths of Plac1 + and Plac1 − malignant epithelial cells with other immune cells. C,D) Pearson correlation of Plac1 + cell count with Treg count in HNSCC tumor tissues. Representative mIF images of Plac1‐low and ‐high samples are shown in (D) (n = 51). Dapi (blue), Plac1 (green), CD4 (red), Foxp3 (grey), in individual and merged channels are shown. Scale bar, 200 µm and 50 µm. E) Bubble plot shows the interaction pairs between Plac1 + and Plac1 − malignant epithelial cells and CD4 T subpopulations. F) Quantification of CXCL11 concentration in supernatant of Plac1‐NC, Plac1‐KO, Plac1‐VEC, and Plac1‐OE HNSCC cells (n = 3). G) Quantification of migrated CD4 + T cells after cocultured with HNSCC cells of different groups (n = 3). H) Representative mIF images show cell–cell interaction of malignant epithelial cells and CD4 + T cells with PVR‐TIGIT pairs. Green: CK5, red: PVR, purple: CD4, grey: TIGIT, blue: Dapi. Scale bar = 50 µm. (I) Representative GO (up) and KEGG pathways (down) enrichment of the predicted target genes expressed in CD4 + T cells by Nichenet algorithm. J,K) Representative flow cytometry images (J) and quantification results (K) of Treg ratio of CD4 + T cells after coculture with Plac1‐NC/KD (up) and Plac1‐VEC/OE (down) HNSCC cells with different treatments (n = 3). P values were calculated by two‐sided Student's t ‐test in F, G, K, by empirical shuffling in E, and by hypergeometric test in I. * p < 0.05, ** p < 0.01, *** p < 0.001.

Journal: Advanced Science

Article Title: Plac1 + Tumor Cell‐Treg Interplay Supports Tumorigenesis and Progression of Head and Neck Cancer

doi: 10.1002/advs.202417312

Figure Lengend Snippet: Plac1 + tumor cells shape the immunosuppressive TME through recruiting CD4 + T cells and promoting Treg differentiation. A) Lollipop plot shows correlation of different immune cells with Plac1 expression in the TCGA‐HNSC cohort. B) Comparison of cell–cell interaction strengths of Plac1 + and Plac1 − malignant epithelial cells with other immune cells. C,D) Pearson correlation of Plac1 + cell count with Treg count in HNSCC tumor tissues. Representative mIF images of Plac1‐low and ‐high samples are shown in (D) (n = 51). Dapi (blue), Plac1 (green), CD4 (red), Foxp3 (grey), in individual and merged channels are shown. Scale bar, 200 µm and 50 µm. E) Bubble plot shows the interaction pairs between Plac1 + and Plac1 − malignant epithelial cells and CD4 T subpopulations. F) Quantification of CXCL11 concentration in supernatant of Plac1‐NC, Plac1‐KO, Plac1‐VEC, and Plac1‐OE HNSCC cells (n = 3). G) Quantification of migrated CD4 + T cells after cocultured with HNSCC cells of different groups (n = 3). H) Representative mIF images show cell–cell interaction of malignant epithelial cells and CD4 + T cells with PVR‐TIGIT pairs. Green: CK5, red: PVR, purple: CD4, grey: TIGIT, blue: Dapi. Scale bar = 50 µm. (I) Representative GO (up) and KEGG pathways (down) enrichment of the predicted target genes expressed in CD4 + T cells by Nichenet algorithm. J,K) Representative flow cytometry images (J) and quantification results (K) of Treg ratio of CD4 + T cells after coculture with Plac1‐NC/KD (up) and Plac1‐VEC/OE (down) HNSCC cells with different treatments (n = 3). P values were calculated by two‐sided Student's t ‐test in F, G, K, by empirical shuffling in E, and by hypergeometric test in I. * p < 0.05, ** p < 0.01, *** p < 0.001.

Article Snippet: Supernatants from Plac1‐OE, Plac1‐KO, and control cells were analyzed using the human CXCL11 ELISA kit (Multi Sciences, #EK1207) following the manufacturer's instructions.

Techniques: Expressing, Comparison, Cell Counting, Concentration Assay, Flow Cytometry

Fig. 7. FABP5 downregulation in DSCs repressed CXCL11/CXCR3 signaling between DSCs and HTR-8/Svneo cells. (A) KEGG pathway analysis of DEGs identified by RNA-seq in FABP5-knockdown primary DSC. (B) Gene Set Enrichment Analysis (GSEA) of chemokine signaling pathways in FABP5-silenced DSCs. (C) FPKM values of CXCL11 expression in control and FABP5-knockdown groups. (D) RT-qPCR, (E, F) Western blot, and (G) ELISA quantification of CXCL11 expression in DSCs transfected with FABP5-targeting or NC siRNAs. (H) RT-qPCR and (I, J) Western blot analyses of CXCR3 expression in HTR-8/Svneo cells treated with CS from FABP5-deficient or control DSCs. Statistical significance: *P < 0.05, **P < 0.01.

Journal: Free radical biology & medicine

Article Title: Oxidative stress-induced decreased expression of FABP5 leads to mitochondrial damage and survival disorder of decidual stromal cells in women with recurrent spontaneous abortion.

doi: 10.1016/j.freeradbiomed.2025.06.003

Figure Lengend Snippet: Fig. 7. FABP5 downregulation in DSCs repressed CXCL11/CXCR3 signaling between DSCs and HTR-8/Svneo cells. (A) KEGG pathway analysis of DEGs identified by RNA-seq in FABP5-knockdown primary DSC. (B) Gene Set Enrichment Analysis (GSEA) of chemokine signaling pathways in FABP5-silenced DSCs. (C) FPKM values of CXCL11 expression in control and FABP5-knockdown groups. (D) RT-qPCR, (E, F) Western blot, and (G) ELISA quantification of CXCL11 expression in DSCs transfected with FABP5-targeting or NC siRNAs. (H) RT-qPCR and (I, J) Western blot analyses of CXCR3 expression in HTR-8/Svneo cells treated with CS from FABP5-deficient or control DSCs. Statistical significance: *P < 0.05, **P < 0.01.

Article Snippet: The concentration of CXCL11 in the CS was measured using a human CXCL11 ELISA kit (Boster, Beijing, China; CAT# EK0737) following the manufacturer’s instructions.

Techniques: RNA Sequencing, Knockdown, Protein-Protein interactions, Expressing, Control, Quantitative RT-PCR, Western Blot, Enzyme-linked Immunosorbent Assay, Transfection

SP-A attenuates antiviral gene expression and chemokine secretion induced by RV-C15. Differentiated NECs were challenged with RV-C15-GFP as described in . mRNA expression of MDA5 , IRF7 , IFNλ , and CXCL11 were quantified by RT-qPCR by using RNA of NECs from non-asthmatics ( n = 6) ( a ) and asthmatics ( n = 10) ( b ). Data are shown as means ± SD from duplicated well in each condition for each donor. Secretion of CXCL11 in apical media was quantified by ELISA in ( c ). The data are means ± SD using cells from 5 non-asthmatic and 6 asthmatic donors; experiments limited by cell availability. p -values were shown in comparison to the condition of RV-C15 48 h alone.

Journal: Viruses

Article Title: Surfactant Protein A Inhibits Human Rhinovirus C Binding and Infection of Airway Epithelial Cells from Pediatric Asthma

doi: 10.3390/v16111709

Figure Lengend Snippet: SP-A attenuates antiviral gene expression and chemokine secretion induced by RV-C15. Differentiated NECs were challenged with RV-C15-GFP as described in . mRNA expression of MDA5 , IRF7 , IFNλ , and CXCL11 were quantified by RT-qPCR by using RNA of NECs from non-asthmatics ( n = 6) ( a ) and asthmatics ( n = 10) ( b ). Data are shown as means ± SD from duplicated well in each condition for each donor. Secretion of CXCL11 in apical media was quantified by ELISA in ( c ). The data are means ± SD using cells from 5 non-asthmatic and 6 asthmatic donors; experiments limited by cell availability. p -values were shown in comparison to the condition of RV-C15 48 h alone.

Article Snippet: The levels of secreted CXCL11 in the apical media were quantified by the human CXCL11 ELISA kit (Peprotech, Cranbury, NJ, USA).

Techniques: Expressing, Quantitative RT-PCR, Enzyme-linked Immunosorbent Assay, Comparison

Journal: iScience

Article Title: Transcriptional synergy in human aortic endothelial cells is vulnerable to combination p300/CBP and BET bromodomain inhibition

doi: 10.1016/j.isci.2024.110011

Figure Lengend Snippet:

Article Snippet: Human CXCL11/I-TAC Quantikine ELISA Kit , Bio-Techne , DCX110.

Techniques: Recombinant, Enzyme-linked Immunosorbent Assay, Isolation, Virus, Sample Prep, SYBR Green Assay, CRISPR, Negative Control, Software, Plasmid Preparation