Fig 1: PC7A initiates CXCL9 expression through STING pathway. (A) Quantification of IFNβ expression in tumor derived CD45+ cells and CD45- cells 24 hours after I.T. treatment of PBS (NC), PC7A, antigen peptide or vaccine (n=3). (B) Quantification of CXCL9 expression in tumor derived CD45+ cells and CD45- cells 24 hours after PC7A, antigen peptide or vaccine I.T. treatment (n=3). (C) Quantification of IFNβ expression in WT and STING-/- mice 24 hours after I.T. treatment (n=4). (D) Quantification of CXCL9 mRNA expression in WT and STING-/- mice 24 hours after PC7A, antigen peptide or vaccine I.T. treatment (n=4). (E) Schematic of STING dependent PC7A induced CXCL9 expression. *P<0.05. One-way ANOVA t-test. ANOVA, analysis of variance; I.T., intratumoral; NS, not significant.
Fig 2: PC7A initiates myeloid cell/CXCL9-CD8+ T/IFNγ feedback loop for T cell recruitment. (A) CXCL9 expression in different cell subpopulations from TC-1 tumors were measured by intracellular staining 24 hours after I.T. vaccination. (B) IFNγ expression in different cell subpopulations from TC-1 tumors were measured by intracellular staining 6 days after I.T. vaccination.(C) Quantification of CXCL9 and IFNγ mRNA expression in TC-1 tumor derived CD45+ cells 24 hours after PC7A, antigen peptide or vaccine I.T. treatment (n=3). (D) Quantification of CXCL9 mRNA in BMDM stimulated with PC7A-antigen or PC7A alone, antigen alone for 24 hours. (E) Intracellular staining of CXCL9+ cells in peritoneal macrophage stimulated with PC7A alone, antigen alone, PC7A-Antigen and IFNγ for 12 hours. (F) Chemotaxis assay of splenocytes derived from tumor bearing mice toward media with or without 900 ng/mL CXCL9. Migrated CD4 + T cells, CD8 + T cells, NK were quantified by flow cytometry. (G) BMDMs in the lower chamber were treatment with 100 µg/mL PC7A or 1 ng/mL IFNγ for 8 hours, chemotaxis assay of splenocytes derived from tumor bearing mice was quantified by flow cytometry. (H) Schematic of myeloid cell/CXCL9-CD8+ T/IFNγ and the effect of PC7A. In panels A–E, I.T. PBS was included as negative control. ****P<0.0001, ***p<0.001, **p<0.01, *p<0.05. One-way ANOVA t-test. ANOVA, analysis of variance; I.T., BMDM, bone marrow-derived macrophage; I.T., intratumoral; NS, not significant.
Fig 3: CXCL9 promotes hepatocyte apoptosis via the AKT pathway. (A) Activities of caspase-3 and (B) caspase-8 in primary WT hepatocytes were elevated following CXCL9 treatment for 4 and 8 h. (C and D) The AKT pathway was activated within the first 5 min of CXCL9 treatment in a time-dependent manner, with the effect lasting up to 8 h. **P<0.01 vs. untreated control. CXCL9, C-X-C motif chemokine ligand-9; AKT, protein kinase B; WT, wild type.
Fig 4: CXCL9 participates in the pathological process of APAP-induced liver injury. (A) Serum levels of CXCL9 were significantly higher in patients who took APAP compared with controls. (B) Compared with mice injected with PBS, those injected with APAP presented increased mRNA levels of CXCL9 lasting up to 12 h. **P<0.01 and ***P<0.001, with comparisons indicated by lines. CXCL9, C-X-C motif chemokine ligand-9; APAP, acetaminophen.
Fig 5: CXCL9 induces CXCR3-mediated apoptosis in mouse liver. (A) At 24 h following intraperitoneal injection of CXCL9, caspase-3 activity in the liver tissues of WT mice was significantly higher compared with the liver tissues of CXCR3−/− mice. (B) Serum levels of ALT and (C) AST were also higher in WT mice injected with CXCL9 compared with CXCR3−/− mice. **P<0.01, ***P<0.001 vs. control. CXCL9, C-X-C motif chemokine ligand-9; CXCR3, C-X-C motif chemokine receptor 3; WT, wild type; ALT, alanine aminotransferase; AST, aspartate aminotransferase.
Supplier Page from Sino Biological, Inc. for Mouse CXCL9 / MIG / C-X-C motif chemokine 9 Protein