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

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

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

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

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

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

Journal: Acta pharmacologica Sinica

Article Title: Pirfenidone ameliorates silica-induced lung inflammation and fibrosis in mice by inhibiting the secretion of interleukin-17A.

doi: 10.1038/s41401-021-00706-4

Figure Lengend Snippet: Fig. 3 Pirfenidone inhibited the secretion of IL-17A in early-stage silicosis models. ELISA was used to detect the protein levels of IL-17A in serum (a) and BALF (b). The mRNA and protein levels of IL-17A in lung tissues from different groups were measured by qPCR (c), immunohistochemistry (d), and Western blot analysis (e). All data were presented as mean ± SD; n = 10 for each group; ***P < 0.001, ****P < 0.0001, ns (no statistical significance).

Article Snippet: IL-17A neutralization By intraperitoneal injection, 100 μg of anti-mouse IL-17A antibody (M00421-2, BOSTER, Wuhan, China) or isotype control IgG (ab18443, abcam, Cambridge, UK) was given to silica-exposed mice weekly for 4 weeks, starting 1 day after silica exposure.

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

Journal: Acta pharmacologica Sinica

Article Title: Pirfenidone ameliorates silica-induced lung inflammation and fibrosis in mice by inhibiting the secretion of interleukin-17A.

doi: 10.1038/s41401-021-00706-4

Figure Lengend Snippet: Fig. 6 Pirfenidone diminished the production of IL-17A in advanced silicosis models. ELISA was performed to measure the protein expression of IL-17A in serum (a) and BALF (b) from different groups. The mRNA and protein levels of IL-17A in lung tissues were measured by qPCR (c), immunohistochemistry (d) and Western blot analysis (e), respectively. All data were presented as mean ± SD; n = 10 for each group; *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001.

Article Snippet: IL-17A neutralization By intraperitoneal injection, 100 μg of anti-mouse IL-17A antibody (M00421-2, BOSTER, Wuhan, China) or isotype control IgG (ab18443, abcam, Cambridge, UK) was given to silica-exposed mice weekly for 4 weeks, starting 1 day after silica exposure.

Techniques: Enzyme-linked Immunosorbent Assay, Expressing, Immunohistochemistry, Western Blot

Journal: Annals of Dermatology

Article Title: Hyaluronan Oligosaccharides Improve Rosacea-Like Phenotype through Anti-Inflammatory and Epidermal Barrier-Improving Effects

doi: 10.5021/ad.2020.32.3.189

Figure Lengend Snippet: Treatment with hyaluronan oligosaccharides (oligo-HAs) reduced inflammatory cell infiltration, interleukin-17 (IL-17), and kallikrein 5 (KLK5) expressions. (A) Hematoxylin and eosin-stained tissue sections of LL-37 induced rosacea-like mice showed marked inflammatory cellular infiltration. Further treatments with oligo-HAs reduced cellular infiltration (H&E, ×100). (B) Majority of infiltrated cells were CD4+ T cells and infiltration of CD4+ T cells decreased in oligo-HAs treated group (CD4, ×100). (C) IL-17A expression was markedly increased in the epidermis of LL-37 induced rosacea-like mice. Oligo-HAs decreased the IL-17A expression regardless of the injection method (IL-17A, ×200). (D) Expression of KLK5 was increased in LL-37 induced rosacea-like mice (arrow head). Further treatment with oligo-HAs reduced KLK5 expression (KLK5, ×400). i.d.: intradermally, i.p.: intraperitoneally.

Article Snippet: To detect CD4, IL-17A, KLK5, filaggrin, and CD44 in histological specimens from mice, primary antibodies including a monoclonal mouse anti-CD4 antibody (BD Biosciences, Franklin Lakes, NJ, USA), monoclonal rat anti-mouse IL-17A antibody (Covalab, Villeurbanne, France), polyclonal rabbit anti-KLK5 antibody (Abcam, Cambridge, UK), polyclonal mouse anti-profilaggrin antibody (Covance, Princeton, NJ, USA), and monoclonal rat anti-human/mice CD44 antibody (eBioscience, San Diego, CA, USA) were used.

Techniques: Staining, Expressing, Injection