anti il 17a monoclonal antibody  (Bio X Cell)

Journal: bioRxiv

Article Title: Th17 effector cytokines induce shared and distinct microglial and endothelial cell responses in post-streptococcal encephalitis

doi: 10.64898/2026.02.04.703836

Figure Lengend Snippet: a–c, Proposed model illustrating how effector cytokines produced by infiltrating Th1 and Th17 lymphocytes following repeated GAS infections may differentially shape transcriptional responses in brain endothelial cells (BECs) and microglia. a, IFNγ is predicted to contribute to the induction of interferon-response programs and antigen-presentation pathways in both microglia and BECs. b,c, IL-17A and GM-CSF appear to exert partially overlapping effects on microglial activation, including regulation of proliferative responses and induction of disease-associated microglial (DAM) genes, cytokines, and chemokines, while also displaying cytokine-specific contributions. Notably, IL-17A signaling may more strongly influence endothelial transcriptional alterations following GAS infections. In addition, antigen-presentation signatures remain elevated in conditions of Th17 deficiency or systemic IL-17A neutralization, suggesting that IL-17A may normally modulate these pathways in both microglia and BECs. Together, these models highlight shared and distinct roles for Th17-associated cytokines in shaping neuroimmune and vascular responses after recurrent GAS exposure.

Article Snippet: Starting 24 hours prior to the first GAS infection, mice were injected intraperitoneally twice weekly with 500 μg of either InVivoMAb anti-mouse IL-17A monoclonal antibody, clone 17F3 (Bio X Cell catalog, BE0173), or mouse IgG1 isotype control monoclonal antibody, clone MOPC-21 (Bio X Cell, catalog BE0083), in 100 μL of dilution buffer (Bio X Cell catalog IP0070 and IP0065, respectively).

Techniques: Produced, Immunopeptidomics, Activation Assay, Neutralization

Journal: bioRxiv

Article Title: Th17 effector cytokines induce shared and distinct microglial and endothelial cell responses in post-streptococcal encephalitis

doi: 10.64898/2026.02.04.703836

Figure Lengend Snippet: a, Timeline of recurrent intranasal GAS infections and administration of an α–IL-17A–neutralizing monoclonal antibody (mAb) or isotype control. b, Heat maps of differentially expressed genes (DEGs) related to BBB function, LPS response, interferon signaling, and antigen presentation in olfactory bulb (OB) brain endothelial cells (BECs) from GAS-infected mice treated with isotype control or α–IL-17A mAb. Values are shown as log(z-score); significantly altered genes are indicated in black (adjusted p < 0.05). c, Gene ontology (GO) pathway enrichment analysis of transcripts upregulated and downregulated in α–IL-17A mAb–treated versus isotype-treated BECs following GAS infections. d, Representative immunofluorescence (IF) images of endogenous IgG leakage (green) in the granular layer of the OB. Blood vessels are labeled with Glut1 (cyan). e, f, Quantification of IgG extravasation (relative fluorescence intensity) in the glomerular ( e ) and granular ( f ) OB layers from PBS- or GAS-infected mice treated with α–IL-17A mAb or isotype control. Comparisons were performed using two-way ANOVA with Šídák’s multiple comparisons test ( p < 0.05; ** p < 0.001; n = 3–7 mice per group). g–i, Representative IF images for IFITM3 (pink), Iba1 (yellow), and CD31 (blue) in the OB of GAS-infected mice treated with isotype or α–IL-17A mAb ( g,h ), and quantification of Ifitm3-positive area within CD31⁺ vasculature ( i ). j,k, Representative fluorescence in situ hybridization (FISH) images of Itm2a mRNA (pink) combined with Glut1 (blue) in the glomerular layer ( j ) and quantification of vascular Itm2a signal ( k ). l, Representative IF images of the tight junction proteins Claudin-5 (green) and ZO-1 (red) in the OB vasculature of GAS-infected mice treated with isotype or α–IL-17A mAb. m, Serum cytokine concentrations measured by multiplex immunoassay in PBS- or GAS-infected mice treated with isotype or α–IL-17A mAb. Data are mean ± SEM. Comparisons were performed using one-way ANOVA with Tukey’s multiple comparisons test (ns, p > 0.05; p < 0.05; * p < 0.01; ** p < 0.001; *** p < 0.0001; n = 3 - 6 mice per group). n, Survival curves of GAS-infected mice treated with isotype control or α–IL-17A mAb (n = 13–48 mice per group). Statistical significance was assessed using the Mantel–Cox log-rank test.

Article Snippet: Starting 24 hours prior to the first GAS infection, mice were injected intraperitoneally twice weekly with 500 μg of either InVivoMAb anti-mouse IL-17A monoclonal antibody, clone 17F3 (Bio X Cell catalog, BE0173), or mouse IgG1 isotype control monoclonal antibody, clone MOPC-21 (Bio X Cell, catalog BE0083), in 100 μL of dilution buffer (Bio X Cell catalog IP0070 and IP0065, respectively).

Techniques: Control, Immunopeptidomics, Olfactory, Infection, Immunofluorescence, Labeling, Fluorescence, In Situ Hybridization, Multiplex Assay