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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
https://www.bioz.com/result/recombinant mouse il 17a f protein/product/R&D Systems
Average 94 stars, based on 162 article reviews

recombinant mouse il 17a f protein - by Bioz Stars, 2026-02

94/100 stars

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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

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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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