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recombinant mouse il 17a f protein (R&D Systems)

Name: recombinant mouse il 17a f protein
Brand: R&D Systems
Rating: 94 (162 reviews)

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R&D Systems recombinant mouse il 17a f protein

<t>IL‐17A</t> and IL‐17F gene and protein expression in lungs of BLM challenged mice. WT mice were treated with saline (CL, white bars) or BLM (grey bars) for 6 h, 24 h, 72 h, 7 days, 14 days, or 21 days, as indicated. (A, B) Gene expression levels of IL‐17A and IL‐17F in sorted TCRαβ pos (A) and TCRγδ pos T cells collected from lungs of BLM‐exposed WT mice. (C, D) Intracellular IL‐17A and IL‐17F protein expression of CD4 pos T cells (C) and TCRγδ pos T cells (D) of WT and IL17af −/− mice was measured 72 h post‐BLM by flow cytometry. (E, F) IL‐17A protein levels in BALF (E) and lung (F) of saline vs. BLM‐treated mice quantified by ELISA. Data are shown as scatter plots with mean values indicated as horizontal lines (A, B) or as mean ± SD of n = 9–12 (A, B), or n = 5–11 (C, D), or n = 4–8 (E, F) mice per group and time point. Note that in A and B, one data point represents a pool of T cells sorted from n = 2–3 mice per experimental group and time point. Data in (C–F) are representative of two independent experiments. * p ≤ 0.05, ** p ≤ 0.01 compared with mice from the control group (Mann–Whitney U ‐test).

Recombinant Mouse Il 17a F Protein, supplied by R&D Systems, used in various techniques. Bioz Stars score: 94/100, based on 162 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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recombinant mouse il 17a f protein - by Bioz Stars, 2026-02

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1) Product Images from "Innate T‐cell‐derived IL‐17A/F protects from bleomycin‐induced acute lung injury but not bleomycin or adenoviral TGF‐β1‐induced lung fibrosis in mice"

Article Title: Innate T‐cell‐derived IL‐17A/F protects from bleomycin‐induced acute lung injury but not bleomycin or adenoviral TGF‐β1‐induced lung fibrosis in mice

Journal: European Journal of Immunology

doi: 10.1002/eji.202451323

IL‐17A and IL‐17F gene and protein expression in lungs of BLM challenged mice. WT mice were treated with saline (CL, white bars) or BLM (grey bars) for 6 h, 24 h, 72 h, 7 days, 14 days, or 21 days, as indicated. (A, B) Gene expression levels of IL‐17A and IL‐17F in sorted TCRαβ pos (A) and TCRγδ pos T cells collected from lungs of BLM‐exposed WT mice. (C, D) Intracellular IL‐17A and IL‐17F protein expression of CD4 pos T cells (C) and TCRγδ pos T cells (D) of WT and IL17af −/− mice was measured 72 h post‐BLM by flow cytometry. (E, F) IL‐17A protein levels in BALF (E) and lung (F) of saline vs. BLM‐treated mice quantified by ELISA. Data are shown as scatter plots with mean values indicated as horizontal lines (A, B) or as mean ± SD of n = 9–12 (A, B), or n = 5–11 (C, D), or n = 4–8 (E, F) mice per group and time point. Note that in A and B, one data point represents a pool of T cells sorted from n = 2–3 mice per experimental group and time point. Data in (C–F) are representative of two independent experiments. * p ≤ 0.05, ** p ≤ 0.01 compared with mice from the control group (Mann–Whitney U ‐test).

Figure Legend Snippet: IL‐17A and IL‐17F gene and protein expression in lungs of BLM challenged mice. WT mice were treated with saline (CL, white bars) or BLM (grey bars) for 6 h, 24 h, 72 h, 7 days, 14 days, or 21 days, as indicated. (A, B) Gene expression levels of IL‐17A and IL‐17F in sorted TCRαβ pos (A) and TCRγδ pos T cells collected from lungs of BLM‐exposed WT mice. (C, D) Intracellular IL‐17A and IL‐17F protein expression of CD4 pos T cells (C) and TCRγδ pos T cells (D) of WT and IL17af −/− mice was measured 72 h post‐BLM by flow cytometry. (E, F) IL‐17A protein levels in BALF (E) and lung (F) of saline vs. BLM‐treated mice quantified by ELISA. Data are shown as scatter plots with mean values indicated as horizontal lines (A, B) or as mean ± SD of n = 9–12 (A, B), or n = 5–11 (C, D), or n = 4–8 (E, F) mice per group and time point. Note that in A and B, one data point represents a pool of T cells sorted from n = 2–3 mice per experimental group and time point. Data in (C–F) are representative of two independent experiments. * p ≤ 0.05, ** p ≤ 0.01 compared with mice from the control group (Mann–Whitney U ‐test).

Techniques Used: Expressing, Saline, Flow Cytometry, Enzyme-linked Immunosorbent Assay, Control, MANN-WHITNEY

Therapy of BLM‐treated IL17af −/− mice with recombinant IL‐17A/F protein. (A) Experimental design. BLM‐exposed IL17af −/− mice were treated i.v. with rIL‐17A/F protein or vehicle, as indicated. (B) Histopathology of hematoxylin/eosin‐stained lung tissue section of IL17af −/− mice with or without rIL‐17A/F protein therapy at day 6 post‐BLM treatment. Closed arrows in (B, left histology) indicate angiocentric neutrophilic infiltrations, while open arrows in (B, left histology) denote intravascular coagulation in IL17af −/− mice treated with BLM for 6 days. Closed arrows in (B, right histology) indicate lymphoplasmacellular infiltrates in BLM‐treated IL17af −/− mice with rIL‐17A/F protein therapy. Representative histology images from a total of n = 4 mice per experimental group are shown at original magnifications of ×40 (Scale bar 20 µm). (C–E) Immunophenotypic analysis of neutrophils (C), CD4 pos T cells (D), and CD8 pos T cells (E) in BALF of BLM‐treated IL17af −/− mice in the absence or presence of rIL‐17A/F protein therapy. Data are shown as mean±SD of n = 5–6 mice per group and time point and are representative of two independent experiments. * p ≤ 0.05, ** p ≤ 0.01 compared with mice from the control group (CL). ++ p ≤ 0.01 rIL‐17A/F application relative to vehicle (Mann–Whitney U ‐test).

Figure Legend Snippet: Therapy of BLM‐treated IL17af −/− mice with recombinant IL‐17A/F protein. (A) Experimental design. BLM‐exposed IL17af −/− mice were treated i.v. with rIL‐17A/F protein or vehicle, as indicated. (B) Histopathology of hematoxylin/eosin‐stained lung tissue section of IL17af −/− mice with or without rIL‐17A/F protein therapy at day 6 post‐BLM treatment. Closed arrows in (B, left histology) indicate angiocentric neutrophilic infiltrations, while open arrows in (B, left histology) denote intravascular coagulation in IL17af −/− mice treated with BLM for 6 days. Closed arrows in (B, right histology) indicate lymphoplasmacellular infiltrates in BLM‐treated IL17af −/− mice with rIL‐17A/F protein therapy. Representative histology images from a total of n = 4 mice per experimental group are shown at original magnifications of ×40 (Scale bar 20 µm). (C–E) Immunophenotypic analysis of neutrophils (C), CD4 pos T cells (D), and CD8 pos T cells (E) in BALF of BLM‐treated IL17af −/− mice in the absence or presence of rIL‐17A/F protein therapy. Data are shown as mean±SD of n = 5–6 mice per group and time point and are representative of two independent experiments. * p ≤ 0.05, ** p ≤ 0.01 compared with mice from the control group (CL). ++ p ≤ 0.01 rIL‐17A/F application relative to vehicle (Mann–Whitney U ‐test).

Techniques Used: Recombinant, Histopathology, Staining, Coagulation, Control, MANN-WHITNEY

AdTGF‐β1 induced lung fibrosis in WT and IL17af −/− mice. WT and IL17af −/− mice were left untreated (grey bars) or were treated with either AdCL (white bars) or AdTGF‐β1 (black bars) for up to 21 days. (A, B) IL‐17A protein levels in BALF (A) and lung (B) of AdCL vs. AdTGF‐β1‐treated mice. (C) Hydroxyproline levels in lung tissue of AdCL‐ vs. AdTGF‐β1‐treated WT and IL17af −/− mice. (D) Histopathology of hematoxylin/eosin‐stained lung tissue sections of WT and IL17af −/− mice at day 14 post‐AdCL vs. AdTGF‐β1 application. Data are shown as mean ± SD of at least n = 5–8 mice per experimental group and time point and are representative of two independent experiments. * p ≤ 0.05, ** p ≤ 0.01 compared with AdCL.

Figure Legend Snippet: AdTGF‐β1 induced lung fibrosis in WT and IL17af −/− mice. WT and IL17af −/− mice were left untreated (grey bars) or were treated with either AdCL (white bars) or AdTGF‐β1 (black bars) for up to 21 days. (A, B) IL‐17A protein levels in BALF (A) and lung (B) of AdCL vs. AdTGF‐β1‐treated mice. (C) Hydroxyproline levels in lung tissue of AdCL‐ vs. AdTGF‐β1‐treated WT and IL17af −/− mice. (D) Histopathology of hematoxylin/eosin‐stained lung tissue sections of WT and IL17af −/− mice at day 14 post‐AdCL vs. AdTGF‐β1 application. Data are shown as mean ± SD of at least n = 5–8 mice per experimental group and time point and are representative of two independent experiments. * p ≤ 0.05, ** p ≤ 0.01 compared with AdCL.

Techniques Used: Histopathology, Staining

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Journal: European Journal of Immunology

Article Title: Innate T‐cell‐derived IL‐17A/F protects from bleomycin‐induced acute lung injury but not bleomycin or adenoviral TGF‐β1‐induced lung fibrosis in mice

doi: 10.1002/eji.202451323

Figure Lengend Snippet: IL‐17A and IL‐17F gene and protein expression in lungs of BLM challenged mice. WT mice were treated with saline (CL, white bars) or BLM (grey bars) for 6 h, 24 h, 72 h, 7 days, 14 days, or 21 days, as indicated. (A, B) Gene expression levels of IL‐17A and IL‐17F in sorted TCRαβ pos (A) and TCRγδ pos T cells collected from lungs of BLM‐exposed WT mice. (C, D) Intracellular IL‐17A and IL‐17F protein expression of CD4 pos T cells (C) and TCRγδ pos T cells (D) of WT and IL17af −/− mice was measured 72 h post‐BLM by flow cytometry. (E, F) IL‐17A protein levels in BALF (E) and lung (F) of saline vs. BLM‐treated mice quantified by ELISA. Data are shown as scatter plots with mean values indicated as horizontal lines (A, B) or as mean ± SD of n = 9–12 (A, B), or n = 5–11 (C, D), or n = 4–8 (E, F) mice per group and time point. Note that in A and B, one data point represents a pool of T cells sorted from n = 2–3 mice per experimental group and time point. Data in (C–F) are representative of two independent experiments. * p ≤ 0.05, ** p ≤ 0.01 compared with mice from the control group (Mann–Whitney U ‐test).

Article Snippet: Recombinant mouse IL‐17A/F protein (rIL‐17A/F) was purchased from R&D Systems.

Techniques: Expressing, Saline, Flow Cytometry, Enzyme-linked Immunosorbent Assay, Control, MANN-WHITNEY

Journal: European Journal of Immunology

Article Title: Innate T‐cell‐derived IL‐17A/F protects from bleomycin‐induced acute lung injury but not bleomycin or adenoviral TGF‐β1‐induced lung fibrosis in mice

doi: 10.1002/eji.202451323

Figure Lengend Snippet: Therapy of BLM‐treated IL17af −/− mice with recombinant IL‐17A/F protein. (A) Experimental design. BLM‐exposed IL17af −/− mice were treated i.v. with rIL‐17A/F protein or vehicle, as indicated. (B) Histopathology of hematoxylin/eosin‐stained lung tissue section of IL17af −/− mice with or without rIL‐17A/F protein therapy at day 6 post‐BLM treatment. Closed arrows in (B, left histology) indicate angiocentric neutrophilic infiltrations, while open arrows in (B, left histology) denote intravascular coagulation in IL17af −/− mice treated with BLM for 6 days. Closed arrows in (B, right histology) indicate lymphoplasmacellular infiltrates in BLM‐treated IL17af −/− mice with rIL‐17A/F protein therapy. Representative histology images from a total of n = 4 mice per experimental group are shown at original magnifications of ×40 (Scale bar 20 µm). (C–E) Immunophenotypic analysis of neutrophils (C), CD4 pos T cells (D), and CD8 pos T cells (E) in BALF of BLM‐treated IL17af −/− mice in the absence or presence of rIL‐17A/F protein therapy. Data are shown as mean±SD of n = 5–6 mice per group and time point and are representative of two independent experiments. * p ≤ 0.05, ** p ≤ 0.01 compared with mice from the control group (CL). ++ p ≤ 0.01 rIL‐17A/F application relative to vehicle (Mann–Whitney U ‐test).

Article Snippet: Recombinant mouse IL‐17A/F protein (rIL‐17A/F) was purchased from R&D Systems.

Techniques: Recombinant, Histopathology, Staining, Coagulation, Control, MANN-WHITNEY

Journal: European Journal of Immunology

Article Title: Innate T‐cell‐derived IL‐17A/F protects from bleomycin‐induced acute lung injury but not bleomycin or adenoviral TGF‐β1‐induced lung fibrosis in mice

doi: 10.1002/eji.202451323

Figure Lengend Snippet: AdTGF‐β1 induced lung fibrosis in WT and IL17af −/− mice. WT and IL17af −/− mice were left untreated (grey bars) or were treated with either AdCL (white bars) or AdTGF‐β1 (black bars) for up to 21 days. (A, B) IL‐17A protein levels in BALF (A) and lung (B) of AdCL vs. AdTGF‐β1‐treated mice. (C) Hydroxyproline levels in lung tissue of AdCL‐ vs. AdTGF‐β1‐treated WT and IL17af −/− mice. (D) Histopathology of hematoxylin/eosin‐stained lung tissue sections of WT and IL17af −/− mice at day 14 post‐AdCL vs. AdTGF‐β1 application. Data are shown as mean ± SD of at least n = 5–8 mice per experimental group and time point and are representative of two independent experiments. * p ≤ 0.05, ** p ≤ 0.01 compared with AdCL.

Article Snippet: Recombinant mouse IL‐17A/F protein (rIL‐17A/F) was purchased from R&D Systems.

Techniques: Histopathology, Staining

HBEC-3KT cells were stimulated with IL-17A/F (50 ng/mL) for 24 h. (A) Cell lysates from cells stimulated with IL- 17A/F and unstimulated cells (14 µg total protein per sample), obtained from five independent experiments (n=5), were independently probed using the high-content aptamer-based proteomic array. Pairwise differential analysis was conducted on normalized log2 protein expression values, and Welch’s t-test with a cutoff of p<0.05 was used to select protein abundance changes that were significantly altered in response to IL-17A/F. (B) TC supernatant collected from cells 24 h post- stimulation was examined for the abundance of LCN-2, Elafin, and GROα, by ELISA. Each dot represents an independent experiment (n=5), and bars show the median and min-max range. Repeated measures one-way ANOVA with Fisher’s least significant difference test was used for statistical analysis ( *p≤0.05, ***p≤0.005 ).

Journal: bioRxiv

Article Title: LL-37 modulates IL-17A/F-mediated airway inflammation by selectively suppressing Lipocalin-2

doi: 10.1101/2024.09.03.610924

Figure Lengend Snippet: HBEC-3KT cells were stimulated with IL-17A/F (50 ng/mL) for 24 h. (A) Cell lysates from cells stimulated with IL- 17A/F and unstimulated cells (14 µg total protein per sample), obtained from five independent experiments (n=5), were independently probed using the high-content aptamer-based proteomic array. Pairwise differential analysis was conducted on normalized log2 protein expression values, and Welch’s t-test with a cutoff of p<0.05 was used to select protein abundance changes that were significantly altered in response to IL-17A/F. (B) TC supernatant collected from cells 24 h post- stimulation was examined for the abundance of LCN-2, Elafin, and GROα, by ELISA. Each dot represents an independent experiment (n=5), and bars show the median and min-max range. Repeated measures one-way ANOVA with Fisher’s least significant difference test was used for statistical analysis ( *p≤0.05, ***p≤0.005 ).

Article Snippet: Recombinant human cytokines IL-17A/F (carrier free) was obtained from R&D Systems (Oakville, ON, CA).

Techniques: Expressing, Enzyme-linked Immunosorbent Assay

HBEC-3KT cells were stimulated with either LL-37, citLL-37 or sLL- 37 (0.25 μM), in the presence and absence of IL-17A/F (50 ng/mL), for 24 h. TC supernatants collected from seven independent experiments (n=7) were examined by ELISA for the abundance LCN-2, Elafin and GROα. Y-axis represents % change compared to paired unstimulated controls. Each dot represents an independent experiment, and bars show the median and min-max range. Each dot is reported as percent (%) change compared to unstimulated cells where % change = ((treatment – control) / control) x 100%. Repeated measures one-way ANOVA with Fisher’s least significant difference test was used for statistical analysis ( *p≤0.05, ****p≤0.0001 ).

Journal: bioRxiv

Article Title: LL-37 modulates IL-17A/F-mediated airway inflammation by selectively suppressing Lipocalin-2

doi: 10.1101/2024.09.03.610924

Figure Lengend Snippet: HBEC-3KT cells were stimulated with either LL-37, citLL-37 or sLL- 37 (0.25 μM), in the presence and absence of IL-17A/F (50 ng/mL), for 24 h. TC supernatants collected from seven independent experiments (n=7) were examined by ELISA for the abundance LCN-2, Elafin and GROα. Y-axis represents % change compared to paired unstimulated controls. Each dot represents an independent experiment, and bars show the median and min-max range. Each dot is reported as percent (%) change compared to unstimulated cells where % change = ((treatment – control) / control) x 100%. Repeated measures one-way ANOVA with Fisher’s least significant difference test was used for statistical analysis ( *p≤0.05, ****p≤0.0001 ).

Article Snippet: Recombinant human cytokines IL-17A/F (carrier free) was obtained from R&D Systems (Oakville, ON, CA).

Techniques: Enzyme-linked Immunosorbent Assay, Control

HBEC- 3KT cells were stimulated with IL-17A/F (50 ng/mL) + TNFα (20 ng/mL) for 24 h. TC supernatants were collected and used in the bottom chamber of transwell plates in a neutrophil migration assays, wherein neutrophils isolated from human blood were used in the upper chamber of the transwell plates. Cell culture medium spiked with human recombinant IL-8 (30 ng/mL) was used as a positive control for neutrophil migration. Results are shown as boxplots with the median line and IQR, and whiskers show minimum and maximum values. Each data point represents an independent experimental replicate with TC supernatant (n=3), using neutrophil isolated from one donor. Each dot represents the average number of neutrophils that traversed the membrane within two hours in each experiment, and bars show the mean and SEM. Repeated measures one-way ANOVA with Fisher’s least significant difference test was used for statistical analysis ( *p≤0.05, **p≤0.01 ).

Journal: bioRxiv

Article Title: LL-37 modulates IL-17A/F-mediated airway inflammation by selectively suppressing Lipocalin-2

doi: 10.1101/2024.09.03.610924

Figure Lengend Snippet: HBEC- 3KT cells were stimulated with IL-17A/F (50 ng/mL) + TNFα (20 ng/mL) for 24 h. TC supernatants were collected and used in the bottom chamber of transwell plates in a neutrophil migration assays, wherein neutrophils isolated from human blood were used in the upper chamber of the transwell plates. Cell culture medium spiked with human recombinant IL-8 (30 ng/mL) was used as a positive control for neutrophil migration. Results are shown as boxplots with the median line and IQR, and whiskers show minimum and maximum values. Each data point represents an independent experimental replicate with TC supernatant (n=3), using neutrophil isolated from one donor. Each dot represents the average number of neutrophils that traversed the membrane within two hours in each experiment, and bars show the mean and SEM. Repeated measures one-way ANOVA with Fisher’s least significant difference test was used for statistical analysis ( *p≤0.05, **p≤0.01 ).

Article Snippet: Recombinant human cytokines IL-17A/F (carrier free) was obtained from R&D Systems (Oakville, ON, CA).

Techniques: Migration, Isolation, Cell Culture, Recombinant, Positive Control, Membrane

HBEC-3KT cells (n=5) were stimulated with either LL-37, citLL-37 or sLL-37 (0.25 μM), in the presence and absence of IL-17A/F (50 ng/mL). mRNA was isolated after (A) 3 h and (B) 6 h, and the mRNA abundance of NGAL2 , NFKBIZ and CEBPB was examined by qRT-PCR. Fold changes (Y-axis) for each gene candidate was normalized to 18S RNA, and compared to unstimulated cells normalized to 1, using the comparative ΔΔCt method. Each data point represents an independent experimental replicate and bars show the mean and SEM. Fisher’s LSD test for one-way ANOVA was used to determine statistical significance ( *p<0.05, **p<0.01, ***p<0.001, ****p<0.0001 ).

Journal: bioRxiv

Article Title: LL-37 modulates IL-17A/F-mediated airway inflammation by selectively suppressing Lipocalin-2

doi: 10.1101/2024.09.03.610924

Figure Lengend Snippet: HBEC-3KT cells (n=5) were stimulated with either LL-37, citLL-37 or sLL-37 (0.25 μM), in the presence and absence of IL-17A/F (50 ng/mL). mRNA was isolated after (A) 3 h and (B) 6 h, and the mRNA abundance of NGAL2 , NFKBIZ and CEBPB was examined by qRT-PCR. Fold changes (Y-axis) for each gene candidate was normalized to 18S RNA, and compared to unstimulated cells normalized to 1, using the comparative ΔΔCt method. Each data point represents an independent experimental replicate and bars show the mean and SEM. Fisher’s LSD test for one-way ANOVA was used to determine statistical significance ( *p<0.05, **p<0.01, ***p<0.001, ****p<0.0001 ).

Article Snippet: Recombinant human cytokines IL-17A/F (carrier free) was obtained from R&D Systems (Oakville, ON, CA).

Techniques: Isolation, Quantitative RT-PCR

Human PBEC obtained from three independent donors (N=3) were stimulated with LL-37, citLL-37, or sLL-37 (0.25 μM), in the presence and absence of IL-17A/F (50 ng/mL). Cell lysates (25 μg total protein per sample) was used to examine the abundance of Regnase-1 (A) 30 minutes and (B) 24 h post-stimulation, by Western blots. (C) The abundance of p-IKKα/β (S176/180) and NF-κB p65, 30 minutes post-stimulation, by Western blots. (D) Human PBEC obtained from three independent donors (N=3) were stimulated with LL- 37, citLL-37, or sLL-37 (0.25 μM), in the presence and absence of IL-17A/F (50 ng/mL) and TNF-α (20 ng/mL). The abundance of LCN-2, 24 h post-stimulation, by ELISA. Y-axis represents % change compared to paired unstimulated cells from each donor. Each dot represents an independent experiment, and bars show the mean and SEM. Each dot is reported as percent (%) change compared to unstimulated PBEC where % change = ((treatment – control) / control) x 100%. Repeated measures one-way ANOVA with Fisher’s least significant difference test was used for statistical analysis ( *p≤0.05 ).

Journal: bioRxiv

Article Title: LL-37 modulates IL-17A/F-mediated airway inflammation by selectively suppressing Lipocalin-2

doi: 10.1101/2024.09.03.610924

Figure Lengend Snippet: Human PBEC obtained from three independent donors (N=3) were stimulated with LL-37, citLL-37, or sLL-37 (0.25 μM), in the presence and absence of IL-17A/F (50 ng/mL). Cell lysates (25 μg total protein per sample) was used to examine the abundance of Regnase-1 (A) 30 minutes and (B) 24 h post-stimulation, by Western blots. (C) The abundance of p-IKKα/β (S176/180) and NF-κB p65, 30 minutes post-stimulation, by Western blots. (D) Human PBEC obtained from three independent donors (N=3) were stimulated with LL- 37, citLL-37, or sLL-37 (0.25 μM), in the presence and absence of IL-17A/F (50 ng/mL) and TNF-α (20 ng/mL). The abundance of LCN-2, 24 h post-stimulation, by ELISA. Y-axis represents % change compared to paired unstimulated cells from each donor. Each dot represents an independent experiment, and bars show the mean and SEM. Each dot is reported as percent (%) change compared to unstimulated PBEC where % change = ((treatment – control) / control) x 100%. Repeated measures one-way ANOVA with Fisher’s least significant difference test was used for statistical analysis ( *p≤0.05 ).

Article Snippet: Recombinant human cytokines IL-17A/F (carrier free) was obtained from R&D Systems (Oakville, ON, CA).

Techniques: Western Blot, Enzyme-linked Immunosorbent Assay, Control

(A) HBEC-3KT cells (n=6) and (B) human PBEC (N=3 independent donors, n=2 technical replicate each) were stimulated with LL-37, citLL-37 or sLL-37 (0.25 μM), in the presence/absence of IL-17A/F (50 ng/mL), for 24 h. TC supernatants were examined for the abundance of CCL20 by ELISA. Y-axis represents % change compared to paired unstimulated cells for each replicate. Each dot represents an independent experiment, and bars show the median and min-max range. Each dot is reported as percent (%) change compared to unstimulated control bronchial epithelial cells where % change = ((treatment – control) / control) x 100%. Repeated measures one-way analysis of variance with Fisher’s least significant difference test was used for statistical analysis ( **p≤0.001, ***p≤0.005, ****p≤0.0001 ).

Journal: bioRxiv

Article Title: LL-37 modulates IL-17A/F-mediated airway inflammation by selectively suppressing Lipocalin-2

doi: 10.1101/2024.09.03.610924

Figure Lengend Snippet: (A) HBEC-3KT cells (n=6) and (B) human PBEC (N=3 independent donors, n=2 technical replicate each) were stimulated with LL-37, citLL-37 or sLL-37 (0.25 μM), in the presence/absence of IL-17A/F (50 ng/mL), for 24 h. TC supernatants were examined for the abundance of CCL20 by ELISA. Y-axis represents % change compared to paired unstimulated cells for each replicate. Each dot represents an independent experiment, and bars show the median and min-max range. Each dot is reported as percent (%) change compared to unstimulated control bronchial epithelial cells where % change = ((treatment – control) / control) x 100%. Repeated measures one-way analysis of variance with Fisher’s least significant difference test was used for statistical analysis ( **p≤0.001, ***p≤0.005, ****p≤0.0001 ).

Article Snippet: Recombinant human cytokines IL-17A/F (carrier free) was obtained from R&D Systems (Oakville, ON, CA).

Techniques: Enzyme-linked Immunosorbent Assay, Control

Female and male BALB/c mice (8-10 weeks; N≥4 per group) were challenged (i.n.) with either saline, 25 μg of HDM protein extract (35 μL of 7 µg/mL saline per mouse) with or without 1 μg LPS (35 μL of 0.03 µg/mL saline per mouse), or LPS alone, once daily for 3 days (days 0 to 2), rested for 4 days followed by HDM allergen recall challenge once daily for 8 consecutive days (as detailed in ). Abundance of (A) CRAMP and (B) IL-17A/F in bronchoalveolar lavage (BAL) was assessed by ELISA, 24 h after the last HDM challenge. (C) Abundance of LCN-2 was assessed in the BALF and lung tissue lysates by ELISA. Bars show median and IQR, whiskers show minimum and maximum points, + denotes average. Statistical analysis was determined by one-way ANOVA with Fisher’s LSD test ( *p≤0.05, **p≤0.001, ***p≤0.005, ****p≤0.0001 ). HDM, house dust mite; LPS, lipopolysaccharide.

Journal: bioRxiv

Article Title: LL-37 modulates IL-17A/F-mediated airway inflammation by selectively suppressing Lipocalin-2

doi: 10.1101/2024.09.03.610924

Figure Lengend Snippet: Female and male BALB/c mice (8-10 weeks; N≥4 per group) were challenged (i.n.) with either saline, 25 μg of HDM protein extract (35 μL of 7 µg/mL saline per mouse) with or without 1 μg LPS (35 μL of 0.03 µg/mL saline per mouse), or LPS alone, once daily for 3 days (days 0 to 2), rested for 4 days followed by HDM allergen recall challenge once daily for 8 consecutive days (as detailed in ). Abundance of (A) CRAMP and (B) IL-17A/F in bronchoalveolar lavage (BAL) was assessed by ELISA, 24 h after the last HDM challenge. (C) Abundance of LCN-2 was assessed in the BALF and lung tissue lysates by ELISA. Bars show median and IQR, whiskers show minimum and maximum points, + denotes average. Statistical analysis was determined by one-way ANOVA with Fisher’s LSD test ( *p≤0.05, **p≤0.001, ***p≤0.005, ****p≤0.0001 ). HDM, house dust mite; LPS, lipopolysaccharide.

Article Snippet: Recombinant human cytokines IL-17A/F (carrier free) was obtained from R&D Systems (Oakville, ON, CA).

Techniques: Saline, Enzyme-linked Immunosorbent Assay

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1) Product Images from "Innate T‐cell‐derived IL‐17A/F protects from bleomycin‐induced acute lung injury but not bleomycin or adenoviral TGF‐β1‐induced lung fibrosis in mice"

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