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: eLife

Article Title: Short-range interactions between fibrocytes and CD8 + T cells in COPD bronchial inflammatory response

doi: 10.7554/eLife.85875

Figure Lengend Snippet:

Article Snippet: Antibody , Anti-IL-17-PE-Cy7 (mouse monoclonal) , Miltenyi Biotec , Cat. #:130-120-413, RRID: AB_2752086 , FC (1:20).

Techniques: Blocking Assay, Recombinant

Journal: Frontiers in Genetics

Article Title: Exosomes containing long non-coding RNA AGAP2-AS1 promote the differentiation of CD4 + T cells through the miR-424-5p/SGK1 axis in psoriasis

doi: 10.3389/fgene.2025.1521470

Figure Lengend Snippet: ASAP2-AS1 promotes the differentiation of Th1 and Th17 in CD4 + T cells and serves as a sponge for miR-424-5p. (A) Fluorescence microscopy was used to detect the subcellular localization of AGAP2-AS1 in CD4 + T cells. AGAP2-AS1 was labeled with Cy3, cell nuclei were counterstained with DAPI (blue). (B) The expression of AGAP2-AS1 in CD4 + T cells after co-incubation of TNF-α-treated HaCaTs-derived exosomes. (C) CD4 + T cells were transfected with LV-AGAP2-AS1 or LV-NC. The percentage of Th1 and Th17 cells was detected by flow cytometry. (D) The protein levels of IFN-γ and IL-17A are measured by ELISA. (E) Prediction of the binding sequence between AGAP2-AS1 and miR-424-5p and construction of the AGAP2-AS1 MUT sequence. (F) Dual-luciferase reporter gene assay confirmed the binding relationship between AGAP2-AS1 and miR-424-5p in HEK-293T cells. (G) AGAP2-AS1 expression level in CD4 + T cells transfected with miR-424-5p mimics or NC mimics and miR-424-5p inhibitor or NC inhibitor. WT wild type, MUT mutant type. Th, T helper. Experiments were repeated three times. *P < 0.05, **P < 0.01, ***P < 0.001. ns: no significance.

Article Snippet: For intracellular cytokine staining, cells were fixed with fixation buffer (E-CK-A109, Elabscience) and then stained intracellularly with antibodies against human IFN-γ (E-AB-F1196C, Elabscience) and IL-17A (E-AB-F1173D, Elabscience).

Techniques: Fluorescence, Microscopy, Labeling, Expressing, Incubation, Derivative Assay, Transfection, Flow Cytometry, Enzyme-linked Immunosorbent Assay, Binding Assay, Sequencing, Luciferase, Reporter Gene Assay, Mutagenesis

Journal: Frontiers in Genetics

Article Title: Exosomes containing long non-coding RNA AGAP2-AS1 promote the differentiation of CD4 + T cells through the miR-424-5p/SGK1 axis in psoriasis

doi: 10.3389/fgene.2025.1521470

Figure Lengend Snippet: AGAP2-AS1/miR-424-5p regulated CD4 + T cell differentiation via the SGK1 signaling pathway. (A) The relative expression levels of SGK1 in 293T cells that were transfected with siRNA targeting SGK1. (B) SGK1 expression level in CD4 + T cells transfected with LV-AGAP2-AS1 or LV-NC and si-AGAP2-AS1 or si-NC. (C) Western blot confirmed that transfection of AGAP2-AS1 in CD4 + T cells promoted the expression of SGK1, and the miR-424-5p mimics reversed this process. (D) Flow cytometry analysis of the percentages of Th1 and Th17 cells in CD4 + T cells transfected with LV-AGAP2-AS1 and miR-424-5p mimics or NC mimics. (E) The protein levels of IFN-γ and IL-17A are measured by ELISA. (F) Flow cytometry analysis of the percentages of Th1 and Th17 cells in CD4 + T cells transfected with LV-AGAP2-AS1 and SGK1 siRNA or NC siRNA. (G) The protein levels of IFN-γ and IL-17A are measured by ELISA. The experiments were repeated three times. *P < 0.05, **P < 0.01, ***P < 0.001.

Article Snippet: For intracellular cytokine staining, cells were fixed with fixation buffer (E-CK-A109, Elabscience) and then stained intracellularly with antibodies against human IFN-γ (E-AB-F1196C, Elabscience) and IL-17A (E-AB-F1173D, Elabscience).

Techniques: Cell Differentiation, Expressing, Transfection, Western Blot, Flow Cytometry, Enzyme-linked Immunosorbent Assay

Journal: Frontiers in Immunology

Article Title: VISTA + follicular regulatory T cells modulate the function of effector immune cells: implications for ovarian cancer immune escape

doi: 10.3389/fimmu.2025.1704048

Figure Lengend Snippet: Effects of VISTA + /VISTA − Tfr cells on CD25 − CD4 + T cell differentiation. (A) Flow cytometry scatter plots showing the effects of VISTA + /VISTA − Tfr cells in the co-culture system on the expression of differentiation markers IFN-γ, IL-4, and IL-17A on CD25 − CD4 + T cells (n=3). (B–D) Quantitative bar graphs showing the expression proportions of Th1, Th2, and Th17 cells after co-culture of CD25 − CD4 + T cells with VISTA − Tfr cells or VISTA − Tfr cells overexpressing VISTA (LV-VISTA). (E–G) Quantitative bar graphs showing the expression proportions of Th1, Th2, and Th17 cells after co-culture of CD25 − CD4 + T cells with VISTA + Tfr cells or VISTA + Tfr cells with VISTA silenced (shRNA-VISTA). The statistical results are expressed as the mean ± SD, * p < 0.05, ** p < 0.01, ns, no significant difference.

Article Snippet: Then, 5 μL each of IL-4-APC (MultiSciences, F11IL403), IFN-γ-PE (MultiSciences, F11IFNG02), and IL-17A-FITC (Elabscience, E-AB-F1173C) antibodies were added, followed by incubation at 4°C in the dark for 30 min.

Techniques: Cell Differentiation, Flow Cytometry, Co-Culture Assay, Expressing, shRNA