anti mouse il 17a Search Results


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MedChemExpress anti mouse rat il 17a antibody
Bioinformatics analysis prioritized PTGS2 and MMP9 as candidate inflammatory genes associated with <t>the</t> <t>IL-17</t> signaling pathway in ischemic stroke. (A) Venn diagram showing the overlap between differentially expressed genes (DEGs) identified from GEO datasets and genes retrieved from the CellAge database. Five overlapping genes were identified: PTGS2, MMP9, SERPINB2, CTNNAL1, and HTRA1. CS, genes from CellAge database; DEG, significantly differentially expressed genes in ischemic stroke. (B) Gene Ontology (GO) enrichment analysis of the overlapping genes, including biological process, cellular component, and molecular function categories. (C) Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis showing that the overlapping genes were enriched in inflammation-related pathways, including the IL-17 signaling pathway and TNF signaling pathway. (D) GSEA comparing ischemic stroke (IS) and control samples, demonstrating enrichment of immune- and inflammation-related pathways in IS. (E) Predicted transcription factor–target gene regulatory network for PTGS2 and MMP9, showing candidate shared upstream transcription factors. Yellow nodes represent TFs, red nodes represent target genes.
Anti Mouse Rat Il 17a Antibody, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Bio X Cell anti il17a
To model EA or MGA respectively, Balb/c or Il4ra -/- mice were given five intranasal (i.n.) challenges with 100ug house dust mite (HDM) extract every week (followed by two days resting) for three consecutive weeks. A final i.n. HDM challenge was given 24 hours prior to harvest. ( A ) Lung sections were stained and representative Masson trichrome (collagen), α-smooth muscle actin (αSMA), and hematoxylin and eosin (H&E) sections and accompanying quantifications are shown. ( B ) Airway resistance to increasing doses of methacholine exposure (6-8 mice per group). (C) Expression of mRNA for IL13 and IL17, assessed by quantitative PCR analyses of lung samples. mRNA expression was calculated relative to GAPDH for 5 mice per group. ( D ) Number of neutrophils or eosinophils in the left lung lobe of EA or MGA induced mice, as assessed by flow cytometry. ( E ) MGA-induced animals were treated with 50ug dexamethasone intratracheally one hour prior to each allergen challenge, beginning on day 7. Lung sections were stained and representative Masson trichrome and αSMA sections and accompanying quantifications are shown. ( F ) Number of neutrophils or eosinophils in the left lung lobe of MGA induced mice treated with or without dexamethasone, as assessed by flow cytometry. ( G ) MGA-induced animals were treated with <t>100ug</t> <t>anti-IL17A</t> or matching isotype control i.p. beginning on day 7 and continuing every other day until harvest. Lung sections were stained, and representative H&E sections and accompanying quantifications are shown. Trichrome data show area of interest values covering full lung section of 6 individual mice per condition. αSMA data show mean values of all bronchi scored from 6 mice per condition. Data are representative of 3 independent experiments. *P < 0.05, **P < 0.005, ***P < 0.0005, ****P < 0.00005; HPF, high-power field; ns, nonsignificant.
Anti Il17a, supplied by Bio X Cell, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Miltenyi Biotec il17a
Figure 3. Effects of iEVs on splenic Th17 cells. Four-month-old female NOD.B10.H2b mice were IV injected with PBS, PD15 iEVs, or PD45 iEVs twice a week for two weeks. Splenocytes were collected at two weeks after last injection. (A,B) Percentages of <t>IL17+</t> cells in splenic CD4+ T cells were examined with flow cytometry. (C) The mRNA levels of Th17 markers <t>(IL17a,</t> IL21, and Rorc) and negative regulator IL1rn in spleen were examined with qRT-PCR. N = 5, ns: not significant, **: p < 0.01, ***: p < 0.001, ****: p < 0.0001.
Il17a, supplied by Miltenyi Biotec, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Elabscience Biotechnology il 17a apc
Figure 3. Effects of iEVs on splenic Th17 cells. Four-month-old female NOD.B10.H2b mice were IV injected with PBS, PD15 iEVs, or PD45 iEVs twice a week for two weeks. Splenocytes were collected at two weeks after last injection. (A,B) Percentages of <t>IL17+</t> cells in splenic CD4+ T cells were examined with flow cytometry. (C) The mRNA levels of Th17 markers <t>(IL17a,</t> IL21, and Rorc) and negative regulator IL1rn in spleen were examined with qRT-PCR. N = 5, ns: not significant, **: p < 0.01, ***: p < 0.001, ****: p < 0.0001.
Il 17a Apc, supplied by Elabscience Biotechnology, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Bio X Cell anti mouse il 17 antibody
Figure 3. Effects of iEVs on splenic Th17 cells. Four-month-old female NOD.B10.H2b mice were IV injected with PBS, PD15 iEVs, or PD45 iEVs twice a week for two weeks. Splenocytes were collected at two weeks after last injection. (A,B) Percentages of <t>IL17+</t> cells in splenic CD4+ T cells were examined with flow cytometry. (C) The mRNA levels of Th17 markers <t>(IL17a,</t> IL21, and Rorc) and negative regulator IL1rn in spleen were examined with qRT-PCR. N = 5, ns: not significant, **: p < 0.01, ***: p < 0.001, ****: p < 0.0001.
Anti Mouse Il 17 Antibody, supplied by Bio X Cell, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Elabscience Biotechnology pe anti mouse il
Figure 3. Effects of iEVs on splenic Th17 cells. Four-month-old female NOD.B10.H2b mice were IV injected with PBS, PD15 iEVs, or PD45 iEVs twice a week for two weeks. Splenocytes were collected at two weeks after last injection. (A,B) Percentages of <t>IL17+</t> cells in splenic CD4+ T cells were examined with flow cytometry. (C) The mRNA levels of Th17 markers <t>(IL17a,</t> IL21, and Rorc) and negative regulator IL1rn in spleen were examined with qRT-PCR. N = 5, ns: not significant, **: p < 0.01, ***: p < 0.001, ****: p < 0.0001.
Pe Anti Mouse Il, supplied by Elabscience Biotechnology, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Elabscience Biotechnology il 17
Figure 3. Effects of iEVs on splenic Th17 cells. Four-month-old female NOD.B10.H2b mice were IV injected with PBS, PD15 iEVs, or PD45 iEVs twice a week for two weeks. Splenocytes were collected at two weeks after last injection. (A,B) Percentages of <t>IL17+</t> cells in splenic CD4+ T cells were examined with flow cytometry. (C) The mRNA levels of Th17 markers <t>(IL17a,</t> IL21, and Rorc) and negative regulator IL1rn in spleen were examined with qRT-PCR. N = 5, ns: not significant, **: p < 0.01, ***: p < 0.001, ****: p < 0.0001.
Il 17, supplied by Elabscience Biotechnology, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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fluidigm anti il 17a
Figure 3. Effects of iEVs on splenic Th17 cells. Four-month-old female NOD.B10.H2b mice were IV injected with PBS, PD15 iEVs, or PD45 iEVs twice a week for two weeks. Splenocytes were collected at two weeks after last injection. (A,B) Percentages of <t>IL17+</t> cells in splenic CD4+ T cells were examined with flow cytometry. (C) The mRNA levels of Th17 markers <t>(IL17a,</t> IL21, and Rorc) and negative regulator IL1rn in spleen were examined with qRT-PCR. N = 5, ns: not significant, **: p < 0.01, ***: p < 0.001, ****: p < 0.0001.
Anti Il 17a, supplied by fluidigm, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Rockland Immunochemicals non competing biotinylated mouse anti human il 17a antibody
Summary of JNJ-8104, golimumab and CNTO 6785 in vitro target-binding kinetics and activities.
Non Competing Biotinylated Mouse Anti Human Il 17a Antibody, supplied by Rockland Immunochemicals, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Elabscience Biotechnology anti mouse il 17a elab fluor 647
Summary of JNJ-8104, golimumab and CNTO 6785 in vitro target-binding kinetics and activities.
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Biogems International anti mouse il 17a
Summary of JNJ-8104, golimumab and CNTO 6785 in vitro target-binding kinetics and activities.
Anti Mouse Il 17a, supplied by Biogems International, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Image Search Results


Bioinformatics analysis prioritized PTGS2 and MMP9 as candidate inflammatory genes associated with the IL-17 signaling pathway in ischemic stroke. (A) Venn diagram showing the overlap between differentially expressed genes (DEGs) identified from GEO datasets and genes retrieved from the CellAge database. Five overlapping genes were identified: PTGS2, MMP9, SERPINB2, CTNNAL1, and HTRA1. CS, genes from CellAge database; DEG, significantly differentially expressed genes in ischemic stroke. (B) Gene Ontology (GO) enrichment analysis of the overlapping genes, including biological process, cellular component, and molecular function categories. (C) Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis showing that the overlapping genes were enriched in inflammation-related pathways, including the IL-17 signaling pathway and TNF signaling pathway. (D) GSEA comparing ischemic stroke (IS) and control samples, demonstrating enrichment of immune- and inflammation-related pathways in IS. (E) Predicted transcription factor–target gene regulatory network for PTGS2 and MMP9, showing candidate shared upstream transcription factors. Yellow nodes represent TFs, red nodes represent target genes.

Journal: Frontiers in Immunology

Article Title: IL-17A-associated PTGS2 and MMP9 inflammatory signaling in ischemic stroke: clinical correlation and experimental evidence

doi: 10.3389/fimmu.2026.1812571

Figure Lengend Snippet: Bioinformatics analysis prioritized PTGS2 and MMP9 as candidate inflammatory genes associated with the IL-17 signaling pathway in ischemic stroke. (A) Venn diagram showing the overlap between differentially expressed genes (DEGs) identified from GEO datasets and genes retrieved from the CellAge database. Five overlapping genes were identified: PTGS2, MMP9, SERPINB2, CTNNAL1, and HTRA1. CS, genes from CellAge database; DEG, significantly differentially expressed genes in ischemic stroke. (B) Gene Ontology (GO) enrichment analysis of the overlapping genes, including biological process, cellular component, and molecular function categories. (C) Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis showing that the overlapping genes were enriched in inflammation-related pathways, including the IL-17 signaling pathway and TNF signaling pathway. (D) GSEA comparing ischemic stroke (IS) and control samples, demonstrating enrichment of immune- and inflammation-related pathways in IS. (E) Predicted transcription factor–target gene regulatory network for PTGS2 and MMP9, showing candidate shared upstream transcription factors. Yellow nodes represent TFs, red nodes represent target genes.

Article Snippet: Rats in the IL-17A neutralizing antibody-treated group were treated with Anti-Mouse/Rat IL-17A Antibody (17F3; MedChemExpress, Cat. No. HY-P990222), a mouse IgG1κ monoclonal neutralizing antibody against mouse/rat IL-17A, via intravenous injection at 100 μg/rat immediately after reperfusion and again at 12 h post-reperfusion.

Techniques: Control

Serum IL-17A, PTGS2, and MMP9 levels in the clinical cohort and their correlations with each other and with stroke severity. (A–C) Serum IL-17A, PTGS2, and MMP9 levels were significantly higher in patients with ischemic stroke than in healthy controls. IS, ischemic stroke (n = 104); Normal, control group (n = 58). (D) Correlations among serum IL-17A, PTGS2, and MMP9 levels in the stroke group. (E) Positive correlations between serum IL-17A, PTGS2, and MMP9 levels and admission NIHSS scores in patients with ischemic stroke. Correlations were analyzed using Spearman’s rank correlation test. *P < 0.05, **P < 0.01, ***P < 0.001.

Journal: Frontiers in Immunology

Article Title: IL-17A-associated PTGS2 and MMP9 inflammatory signaling in ischemic stroke: clinical correlation and experimental evidence

doi: 10.3389/fimmu.2026.1812571

Figure Lengend Snippet: Serum IL-17A, PTGS2, and MMP9 levels in the clinical cohort and their correlations with each other and with stroke severity. (A–C) Serum IL-17A, PTGS2, and MMP9 levels were significantly higher in patients with ischemic stroke than in healthy controls. IS, ischemic stroke (n = 104); Normal, control group (n = 58). (D) Correlations among serum IL-17A, PTGS2, and MMP9 levels in the stroke group. (E) Positive correlations between serum IL-17A, PTGS2, and MMP9 levels and admission NIHSS scores in patients with ischemic stroke. Correlations were analyzed using Spearman’s rank correlation test. *P < 0.05, **P < 0.01, ***P < 0.001.

Article Snippet: Rats in the IL-17A neutralizing antibody-treated group were treated with Anti-Mouse/Rat IL-17A Antibody (17F3; MedChemExpress, Cat. No. HY-P990222), a mouse IgG1κ monoclonal neutralizing antibody against mouse/rat IL-17A, via intravenous injection at 100 μg/rat immediately after reperfusion and again at 12 h post-reperfusion.

Techniques: Control

MCAO-induced activation of IL-17A/PTGS2/MMP9-related inflammatory markers and changes after anti-IL-17A antibody treatment in rat brain tissue. (A–C) Relative mRNA levels of PTGS2, MMP9, and IL-17A in the sham, MCAO, and anti-IL-17A Ab groups. (D–F) Protein concentrations of PTGS2, MMP9, and IL-17A. (G, H) Concentrations of PGE2 and IL-6. (I) Neurological deficit scores assessed using the Longa scoring system. In panel I, the sham group median was 0; therefore, a minimal bar height was displayed for visualization only. (J) Representative TTC-stained brain sections from the MCAO and anti-IL-17A Ab groups. White areas indicate infarct regions, whereas red areas indicate viable brain tissue. (K) Quantitative analysis of infarct volume percentage based on TTC staining. Sham, sham-operated group; Model, MCAO group; anti-IL-17A Ab, IL-17A neutralizing antibody-treated MCAO group. Data in panels A-H are presented as mean ± SEM (n = 6 per group). Neurological deficit scores in panel I are presented as median (interquartile range) (n = 6 per group). TTC analysis in panels (J, K) was performed in an independent cohort of rats, with final sample sizes of n = 4 for the MCAO group and n = 5 for the anti-IL-17A Ab group; one rat in the MCAO group died before tissue collection. *P < 0.05, **P < 0.01, ***P < 0.001.

Journal: Frontiers in Immunology

Article Title: IL-17A-associated PTGS2 and MMP9 inflammatory signaling in ischemic stroke: clinical correlation and experimental evidence

doi: 10.3389/fimmu.2026.1812571

Figure Lengend Snippet: MCAO-induced activation of IL-17A/PTGS2/MMP9-related inflammatory markers and changes after anti-IL-17A antibody treatment in rat brain tissue. (A–C) Relative mRNA levels of PTGS2, MMP9, and IL-17A in the sham, MCAO, and anti-IL-17A Ab groups. (D–F) Protein concentrations of PTGS2, MMP9, and IL-17A. (G, H) Concentrations of PGE2 and IL-6. (I) Neurological deficit scores assessed using the Longa scoring system. In panel I, the sham group median was 0; therefore, a minimal bar height was displayed for visualization only. (J) Representative TTC-stained brain sections from the MCAO and anti-IL-17A Ab groups. White areas indicate infarct regions, whereas red areas indicate viable brain tissue. (K) Quantitative analysis of infarct volume percentage based on TTC staining. Sham, sham-operated group; Model, MCAO group; anti-IL-17A Ab, IL-17A neutralizing antibody-treated MCAO group. Data in panels A-H are presented as mean ± SEM (n = 6 per group). Neurological deficit scores in panel I are presented as median (interquartile range) (n = 6 per group). TTC analysis in panels (J, K) was performed in an independent cohort of rats, with final sample sizes of n = 4 for the MCAO group and n = 5 for the anti-IL-17A Ab group; one rat in the MCAO group died before tissue collection. *P < 0.05, **P < 0.01, ***P < 0.001.

Article Snippet: Rats in the IL-17A neutralizing antibody-treated group were treated with Anti-Mouse/Rat IL-17A Antibody (17F3; MedChemExpress, Cat. No. HY-P990222), a mouse IgG1κ monoclonal neutralizing antibody against mouse/rat IL-17A, via intravenous injection at 100 μg/rat immediately after reperfusion and again at 12 h post-reperfusion.

Techniques: Activation Assay, Staining

Spearman correlation analyses among IL-17A, PTGS2, MMP9, PGE2, and IL-6 in rat brain tissue. Correlation analyses were performed using pooled data from all animals (n = 18). (A) Correlation between IL-17A and PTGS2 mRNA expression. (B) Correlation between IL-17A and MMP9 mRNA expression. (C) Correlation between IL-17A and PTGS2 protein expression. (D) Correlation between IL-17A and MMP9 protein expression. (E) Correlation between IL-17A and PGE2 levels. (F) Correlation between IL-17A and IL-6 levels. Sham, sham-operated group; Model, MCAO group; anti-IL-17A Ab, IL-17A neutralizing antibody-treated MCAO group. Given the limited sample size, these correlations should be interpreted with caution.

Journal: Frontiers in Immunology

Article Title: IL-17A-associated PTGS2 and MMP9 inflammatory signaling in ischemic stroke: clinical correlation and experimental evidence

doi: 10.3389/fimmu.2026.1812571

Figure Lengend Snippet: Spearman correlation analyses among IL-17A, PTGS2, MMP9, PGE2, and IL-6 in rat brain tissue. Correlation analyses were performed using pooled data from all animals (n = 18). (A) Correlation between IL-17A and PTGS2 mRNA expression. (B) Correlation between IL-17A and MMP9 mRNA expression. (C) Correlation between IL-17A and PTGS2 protein expression. (D) Correlation between IL-17A and MMP9 protein expression. (E) Correlation between IL-17A and PGE2 levels. (F) Correlation between IL-17A and IL-6 levels. Sham, sham-operated group; Model, MCAO group; anti-IL-17A Ab, IL-17A neutralizing antibody-treated MCAO group. Given the limited sample size, these correlations should be interpreted with caution.

Article Snippet: Rats in the IL-17A neutralizing antibody-treated group were treated with Anti-Mouse/Rat IL-17A Antibody (17F3; MedChemExpress, Cat. No. HY-P990222), a mouse IgG1κ monoclonal neutralizing antibody against mouse/rat IL-17A, via intravenous injection at 100 μg/rat immediately after reperfusion and again at 12 h post-reperfusion.

Techniques: Expressing

To model EA or MGA respectively, Balb/c or Il4ra -/- mice were given five intranasal (i.n.) challenges with 100ug house dust mite (HDM) extract every week (followed by two days resting) for three consecutive weeks. A final i.n. HDM challenge was given 24 hours prior to harvest. ( A ) Lung sections were stained and representative Masson trichrome (collagen), α-smooth muscle actin (αSMA), and hematoxylin and eosin (H&E) sections and accompanying quantifications are shown. ( B ) Airway resistance to increasing doses of methacholine exposure (6-8 mice per group). (C) Expression of mRNA for IL13 and IL17, assessed by quantitative PCR analyses of lung samples. mRNA expression was calculated relative to GAPDH for 5 mice per group. ( D ) Number of neutrophils or eosinophils in the left lung lobe of EA or MGA induced mice, as assessed by flow cytometry. ( E ) MGA-induced animals were treated with 50ug dexamethasone intratracheally one hour prior to each allergen challenge, beginning on day 7. Lung sections were stained and representative Masson trichrome and αSMA sections and accompanying quantifications are shown. ( F ) Number of neutrophils or eosinophils in the left lung lobe of MGA induced mice treated with or without dexamethasone, as assessed by flow cytometry. ( G ) MGA-induced animals were treated with 100ug anti-IL17A or matching isotype control i.p. beginning on day 7 and continuing every other day until harvest. Lung sections were stained, and representative H&E sections and accompanying quantifications are shown. Trichrome data show area of interest values covering full lung section of 6 individual mice per condition. αSMA data show mean values of all bronchi scored from 6 mice per condition. Data are representative of 3 independent experiments. *P < 0.05, **P < 0.005, ***P < 0.0005, ****P < 0.00005; HPF, high-power field; ns, nonsignificant.

Journal: bioRxiv

Article Title: The metabolic reprogramming of T cells controls airway remodeling in severe asthma

doi: 10.64898/2026.03.19.712985

Figure Lengend Snippet: To model EA or MGA respectively, Balb/c or Il4ra -/- mice were given five intranasal (i.n.) challenges with 100ug house dust mite (HDM) extract every week (followed by two days resting) for three consecutive weeks. A final i.n. HDM challenge was given 24 hours prior to harvest. ( A ) Lung sections were stained and representative Masson trichrome (collagen), α-smooth muscle actin (αSMA), and hematoxylin and eosin (H&E) sections and accompanying quantifications are shown. ( B ) Airway resistance to increasing doses of methacholine exposure (6-8 mice per group). (C) Expression of mRNA for IL13 and IL17, assessed by quantitative PCR analyses of lung samples. mRNA expression was calculated relative to GAPDH for 5 mice per group. ( D ) Number of neutrophils or eosinophils in the left lung lobe of EA or MGA induced mice, as assessed by flow cytometry. ( E ) MGA-induced animals were treated with 50ug dexamethasone intratracheally one hour prior to each allergen challenge, beginning on day 7. Lung sections were stained and representative Masson trichrome and αSMA sections and accompanying quantifications are shown. ( F ) Number of neutrophils or eosinophils in the left lung lobe of MGA induced mice treated with or without dexamethasone, as assessed by flow cytometry. ( G ) MGA-induced animals were treated with 100ug anti-IL17A or matching isotype control i.p. beginning on day 7 and continuing every other day until harvest. Lung sections were stained, and representative H&E sections and accompanying quantifications are shown. Trichrome data show area of interest values covering full lung section of 6 individual mice per condition. αSMA data show mean values of all bronchi scored from 6 mice per condition. Data are representative of 3 independent experiments. *P < 0.05, **P < 0.005, ***P < 0.0005, ****P < 0.00005; HPF, high-power field; ns, nonsignificant.

Article Snippet: To block IL-17 signaling, 100ug anti-IL17A (17F3; BioXCell) or matching isotype control (MOPC-21; BioXCell) were given intraperitoneally (i.p.) to HDM induced Ilr4a -/- mice beginning on day 7 and continuing every other day for a total of 7 injections.

Techniques: Staining, Expressing, Real-time Polymerase Chain Reaction, Flow Cytometry, Control

Figure 3. Effects of iEVs on splenic Th17 cells. Four-month-old female NOD.B10.H2b mice were IV injected with PBS, PD15 iEVs, or PD45 iEVs twice a week for two weeks. Splenocytes were collected at two weeks after last injection. (A,B) Percentages of IL17+ cells in splenic CD4+ T cells were examined with flow cytometry. (C) The mRNA levels of Th17 markers (IL17a, IL21, and Rorc) and negative regulator IL1rn in spleen were examined with qRT-PCR. N = 5, ns: not significant, **: p < 0.01, ***: p < 0.001, ****: p < 0.0001.

Journal: International journal of molecular sciences

Article Title: Inhibitory Effects of Extracellular Vesicles from iPS-Cell-Derived Mesenchymal Stem Cells on the Onset of Sialadenitis in Sjögren's Syndrome Are Mediated by Immunomodulatory Splenocytes and Improved by Inhibiting miR-125b.

doi: 10.3390/ijms24065258

Figure Lengend Snippet: Figure 3. Effects of iEVs on splenic Th17 cells. Four-month-old female NOD.B10.H2b mice were IV injected with PBS, PD15 iEVs, or PD45 iEVs twice a week for two weeks. Splenocytes were collected at two weeks after last injection. (A,B) Percentages of IL17+ cells in splenic CD4+ T cells were examined with flow cytometry. (C) The mRNA levels of Th17 markers (IL17a, IL21, and Rorc) and negative regulator IL1rn in spleen were examined with qRT-PCR. N = 5, ns: not significant, **: p < 0.01, ***: p < 0.001, ****: p < 0.0001.

Article Snippet: These cells were stained with fluorescent-labeled antibodies against F4/80 (BD Pharmingen 123116, 123107, San Diego, CA, USA), CD3 (BioLegend 100236, San Diego, CA, USA), CD19 (BioLegend 152409), CD38 (BioLegend 102707), CD206 (BioLegend 141706), CD4 (BioLegend 100408), IL17a (130-112-009, Miltenyi Biotec, San Diego, CA, USA), or the corresponding isotype controls (BioLegend 400608, 400511, 400612, 400207, 1:100).

Techniques: Injection, Cytometry, Quantitative RT-PCR

Figure 6. Effects of inhibiting miR-125b in aging iEVs on the polarization of splenic macrophages. Four-month-old female NOD.B10.H2b mice were IV injected with PBS, Ctrl EVs, or 125KD EVs twice a week for two weeks. Splenocytes were collected at two weeks after last injection. (A,B) Percentages of IL17+ cells in CD4+ splenocytes were examined with flow cytometry. (C) The mRNA levels of Th17 markers (IL17a, IL21, and Rorc) and negative regulator IL1rn in spleen were examined with qRT-PCR. N = 5, ns: not significant, *: p < 0.05, **: p < 0.01, ****: p < 0.0001.

Journal: International journal of molecular sciences

Article Title: Inhibitory Effects of Extracellular Vesicles from iPS-Cell-Derived Mesenchymal Stem Cells on the Onset of Sialadenitis in Sjögren's Syndrome Are Mediated by Immunomodulatory Splenocytes and Improved by Inhibiting miR-125b.

doi: 10.3390/ijms24065258

Figure Lengend Snippet: Figure 6. Effects of inhibiting miR-125b in aging iEVs on the polarization of splenic macrophages. Four-month-old female NOD.B10.H2b mice were IV injected with PBS, Ctrl EVs, or 125KD EVs twice a week for two weeks. Splenocytes were collected at two weeks after last injection. (A,B) Percentages of IL17+ cells in CD4+ splenocytes were examined with flow cytometry. (C) The mRNA levels of Th17 markers (IL17a, IL21, and Rorc) and negative regulator IL1rn in spleen were examined with qRT-PCR. N = 5, ns: not significant, *: p < 0.05, **: p < 0.01, ****: p < 0.0001.

Article Snippet: These cells were stained with fluorescent-labeled antibodies against F4/80 (BD Pharmingen 123116, 123107, San Diego, CA, USA), CD3 (BioLegend 100236, San Diego, CA, USA), CD19 (BioLegend 152409), CD38 (BioLegend 102707), CD206 (BioLegend 141706), CD4 (BioLegend 100408), IL17a (130-112-009, Miltenyi Biotec, San Diego, CA, USA), or the corresponding isotype controls (BioLegend 400608, 400511, 400612, 400207, 1:100).

Techniques: Injection, Cytometry, Quantitative RT-PCR

Summary of JNJ-8104, golimumab and CNTO 6785 in vitro target-binding kinetics and activities.

Journal: mAbs

Article Title: Characterization of concurrent target suppression by JNJ-61178104, a bispecific antibody against human tumor necrosis factor and interleukin-17A

doi: 10.1080/19420862.2020.1770018

Figure Lengend Snippet: Summary of JNJ-8104, golimumab and CNTO 6785 in vitro target-binding kinetics and activities.

Article Snippet: The concentrations of total IL-17A in cyno and human serum were measured with similar MSD assays, except using a non-competing biotinylated mouse anti-human IL-17A antibody (Clone 4H1524.1, Rockland) for capture and a non-competing ruthenium-labeled mouse IgG1 anti-human IL-17A antibody (Clone 41802, R&D Systems) for detection.

Techniques: In Vitro

Inhibition of in vitro inflammatory responses mediated by endogenous TNF and IL-17A. Human rheumatoid arthritis fibroblast-like synovial cells (RA-FLS) were cocultured with in vitro differentiated T h 17/T h 1 cells. Various concentrations of JNJ-8104, CNTO 9809 (parental anti-TNF), CNTO 4782 (parental anti-IL-17A) or equal-molar fixed-ratio combination of CNTO 9809 and CNTO 4782 were incubated with the coculture for 48 hours. Endogenous TNF and IL-17A-mediated production of IL-6 (a) and GROα (b) in the supernatants were measured.

Journal: mAbs

Article Title: Characterization of concurrent target suppression by JNJ-61178104, a bispecific antibody against human tumor necrosis factor and interleukin-17A

doi: 10.1080/19420862.2020.1770018

Figure Lengend Snippet: Inhibition of in vitro inflammatory responses mediated by endogenous TNF and IL-17A. Human rheumatoid arthritis fibroblast-like synovial cells (RA-FLS) were cocultured with in vitro differentiated T h 17/T h 1 cells. Various concentrations of JNJ-8104, CNTO 9809 (parental anti-TNF), CNTO 4782 (parental anti-IL-17A) or equal-molar fixed-ratio combination of CNTO 9809 and CNTO 4782 were incubated with the coculture for 48 hours. Endogenous TNF and IL-17A-mediated production of IL-6 (a) and GROα (b) in the supernatants were measured.

Article Snippet: The concentrations of total IL-17A in cyno and human serum were measured with similar MSD assays, except using a non-competing biotinylated mouse anti-human IL-17A antibody (Clone 4H1524.1, Rockland) for capture and a non-competing ruthenium-labeled mouse IgG1 anti-human IL-17A antibody (Clone 41802, R&D Systems) for detection.

Techniques: Inhibition, In Vitro, Incubation

Inhibition of rhTNF- and rhIL-17A-induced Cellular Influx by JNJ-8104 in the Airway Lumen of Mice. Mice were intranasally instilled with rhTNF- and rhIL-17A in combination. After 6 h their lungs were lavaged and total numbers of BAL cells (a) and neutrophils (b) were enumerated as detailed in “Materials & Methods.” Mice were injected intraperitoneally with the test mAbs or isotype control18 hours prior to cytokines challenge. Data are represented as mean ± SEM; N = 6–7 mice/group.

Journal: mAbs

Article Title: Characterization of concurrent target suppression by JNJ-61178104, a bispecific antibody against human tumor necrosis factor and interleukin-17A

doi: 10.1080/19420862.2020.1770018

Figure Lengend Snippet: Inhibition of rhTNF- and rhIL-17A-induced Cellular Influx by JNJ-8104 in the Airway Lumen of Mice. Mice were intranasally instilled with rhTNF- and rhIL-17A in combination. After 6 h their lungs were lavaged and total numbers of BAL cells (a) and neutrophils (b) were enumerated as detailed in “Materials & Methods.” Mice were injected intraperitoneally with the test mAbs or isotype control18 hours prior to cytokines challenge. Data are represented as mean ± SEM; N = 6–7 mice/group.

Article Snippet: The concentrations of total IL-17A in cyno and human serum were measured with similar MSD assays, except using a non-competing biotinylated mouse anti-human IL-17A antibody (Clone 4H1524.1, Rockland) for capture and a non-competing ruthenium-labeled mouse IgG1 anti-human IL-17A antibody (Clone 41802, R&D Systems) for detection.

Techniques: Inhibition, Injection

Observed serum concentrations versus time profiles of Total mAb (a), total TNF (b), and Total IL-17A (c) following IV administration of golimumab (parental anti-TNF), CNTO 6785 (anti-IL-17A with identical parental Fab arms) or JNJ-8104 at the specified dose levels in cynomolgus monkeys. Data are represented as mean ± SD.

Journal: mAbs

Article Title: Characterization of concurrent target suppression by JNJ-61178104, a bispecific antibody against human tumor necrosis factor and interleukin-17A

doi: 10.1080/19420862.2020.1770018

Figure Lengend Snippet: Observed serum concentrations versus time profiles of Total mAb (a), total TNF (b), and Total IL-17A (c) following IV administration of golimumab (parental anti-TNF), CNTO 6785 (anti-IL-17A with identical parental Fab arms) or JNJ-8104 at the specified dose levels in cynomolgus monkeys. Data are represented as mean ± SD.

Article Snippet: The concentrations of total IL-17A in cyno and human serum were measured with similar MSD assays, except using a non-competing biotinylated mouse anti-human IL-17A antibody (Clone 4H1524.1, Rockland) for capture and a non-competing ruthenium-labeled mouse IgG1 anti-human IL-17A antibody (Clone 41802, R&D Systems) for detection.

Techniques:

Estimated JNJ-8104, CNTO148 and CNTO 6785 cynomolgus monkey PK/TE model parameters (mean, residual standard error%) and predicted human parameters.

Journal: mAbs

Article Title: Characterization of concurrent target suppression by JNJ-61178104, a bispecific antibody against human tumor necrosis factor and interleukin-17A

doi: 10.1080/19420862.2020.1770018

Figure Lengend Snippet: Estimated JNJ-8104, CNTO148 and CNTO 6785 cynomolgus monkey PK/TE model parameters (mean, residual standard error%) and predicted human parameters.

Article Snippet: The concentrations of total IL-17A in cyno and human serum were measured with similar MSD assays, except using a non-competing biotinylated mouse anti-human IL-17A antibody (Clone 4H1524.1, Rockland) for capture and a non-competing ruthenium-labeled mouse IgG1 anti-human IL-17A antibody (Clone 41802, R&D Systems) for detection.

Techniques:

PK/TE model fitting of PK, total IL-17A and Free IL-17A profiles following IV administration of JNJ-8104 (a) and CNTO 6785 (b) in cynomolgus monkeys. Symbols = Observed individual data; Lines = Mean model prediction.

Journal: mAbs

Article Title: Characterization of concurrent target suppression by JNJ-61178104, a bispecific antibody against human tumor necrosis factor and interleukin-17A

doi: 10.1080/19420862.2020.1770018

Figure Lengend Snippet: PK/TE model fitting of PK, total IL-17A and Free IL-17A profiles following IV administration of JNJ-8104 (a) and CNTO 6785 (b) in cynomolgus monkeys. Symbols = Observed individual data; Lines = Mean model prediction.

Article Snippet: The concentrations of total IL-17A in cyno and human serum were measured with similar MSD assays, except using a non-competing biotinylated mouse anti-human IL-17A antibody (Clone 4H1524.1, Rockland) for capture and a non-competing ruthenium-labeled mouse IgG1 anti-human IL-17A antibody (Clone 41802, R&D Systems) for detection.

Techniques:

Comparison of observed and model-predicted Total IL-17A profiles following a single IV administration of JNJ-8104 at 0.1, 0.3, 1, 3 and 10 mg/kg (a−e) normal human subjects. Symbols = Observed individual data; Solid lines = Mean model prediction based on cyno PK/TE model parameters and allometric scaling for human PK; Dotted lines = Mean model prediction based on estimated JNJ-8104 human PK parameters from FIH data with cyno-based in vivo KD.

Journal: mAbs

Article Title: Characterization of concurrent target suppression by JNJ-61178104, a bispecific antibody against human tumor necrosis factor and interleukin-17A

doi: 10.1080/19420862.2020.1770018

Figure Lengend Snippet: Comparison of observed and model-predicted Total IL-17A profiles following a single IV administration of JNJ-8104 at 0.1, 0.3, 1, 3 and 10 mg/kg (a−e) normal human subjects. Symbols = Observed individual data; Solid lines = Mean model prediction based on cyno PK/TE model parameters and allometric scaling for human PK; Dotted lines = Mean model prediction based on estimated JNJ-8104 human PK parameters from FIH data with cyno-based in vivo KD.

Article Snippet: The concentrations of total IL-17A in cyno and human serum were measured with similar MSD assays, except using a non-competing biotinylated mouse anti-human IL-17A antibody (Clone 4H1524.1, Rockland) for capture and a non-competing ruthenium-labeled mouse IgG1 anti-human IL-17A antibody (Clone 41802, R&D Systems) for detection.

Techniques: Comparison, In Vivo