CXCL10 Antibody - #DF6417

Fig. 5. CXCL10 sensitizes neurons to ferroptosis in vivo. (A) The gene profiles associated with astrocyte phenotype. (B) The protein level of CXCL10 in the epileptic brains using ELISA. (C) CXCR3 expression was determined via Western blot analysis. (D-E) Confocal microscopy was used to show the colocalization of GFAP/CXCL10 and CXCR3/GPX4 in the CA3 region of epilepsy. (F) The coordinates for the lateral ventricle injection in the murine brain. Behavior recordings of models after PTZ kindling, including (G) seizure scores, (H) GTCs latency, and (I) GTCs duration. (J) Various ferroptosis-related mRNAs (Ptgs2, Rpl8, Dpp4, and Chac1) were measured via qPCR. (K) Western blot showing the levels of CXCR3, GPX4, DPP4, and 4-HNE in mice treated with recombinant CXCL10. (L) Immunofluorescence staining showed the protein level of GPX4 in the CA3 region after treatment with recombinant CXCL10. (M) Immunohistochemistry staining of NeuN revealed the neuronal injury. Data are expressed as the mean ± SEM. *P < 0.05, **P < 0.01, ***P < 0.001. The scale bar represents 50 μm.

Fig. 3 The expression of CXCL9 and CXCL10 are highly activated by S. aureus challenge in bone marrow monocytes of 8-week-old mice. (a) Gene ontology (GO) enrichment analysis of biological processes for upregulated differentially expressed genes (DEGs). The transcriptome data of S. aureus-infected bone and control ones in young mice on day 3 after surgery (GSE166522) were analyzed by bioinformatics. (b) Venn diagram of overlapping DEGs between cytokine-mediated signaling pathway and response to molecule of bacterial origin. (c) Heatmap of 12 overlapping DEGs. (d) mRNA expression of the top 3 highly up-regulated genes (CXCL9, IL-1β, CXCL10) in bone tissue on day 3 after surgery. n = 4/ group. One-way ANOVA with Dunnett’s T3 post hoc test, *p 

Figure 7. Verification of PLAC8 expression and immune cell infiltration in verified cohort. (A) Representative results of protein expression levels of PLAC8, CXCL10 and 7 immune cell markers in IC/BPS tissue and UC tissue (Microscale: 100 μm). (B) The IHC score of PLAC8 in IC/BPS tissues and UC tissues. (C) The IHC score of CXCL10 in IC/BPS tissues and UC tissues. (D) Number of positive cells for seven immune cell marker in IC/BPS tissues and UC tissues. (E) The relative proportions of seven immune cell marker’s protein expression in IC/BPS tissues and UC tissues. IC/BPS, interstitial cystitis/painful bladder syndrome; UC, unaffected control; IHC, Immunohistochemistry. **P 

Fig 5 Splenic and cerebral T cell population changes in hApoE2 and hApoE3 mice after PbA infection. (A) Representative flow cytometric plots showing splenic CD4+ and CD8+ T cells on days 0 and 5 of PbA-infected hApoE2 and hApoE3 mice. (B and C) Percentages (left panel) and absolute numbers (right panel) of splenic CD4+ and CD8+ T cells from PbA-infected mice. n = 4 mice per group. (D) Representative flow cytometric plots showing cerebral CD4+ and CD8+ T cells on days 0 and 5 of PbA-infected hApoE2 and hApoE3 mice. (E and F) Percentages (left panel) and absolute numbers (right panel) of cerebral CD4+ and CD8+ T cells from PbA-infected mice. n = 4 mice per group. (G) Western blots of CXCR3, CXCL9, and CXCL10 in the brain from uninfected and PbA-infected hApoE2 and hApoE3 mice on day 5 pi. (H) Densitometric quantification of CXCR3, CXCL9, and CXCL10 expression in panel G, respectively; band densities were normalized to β-actin. n = 3 experimental repeats. (B, C, E, and F) Mann-Whitney test; (H) Tukey’s multiple comparisons test (CXCR3), and unpaired t-test (CXCL9, CXCL10). *P < 0.05; **P < 0.01; and ***P < 0.001.

Figure 5. PTB mediated MMT through CXCL10. (A) Gene expression difference of volcano plot between Sham and UUO. (B) Gene expression difference of volcano plot between UUO and PTB treatment. (C) Venn plot suggests that 11 genes may play a role in the inhibition of RIF by PTB. (D) Heatmap analysis. (E) The verification of 11 genes by RT-PCR. (F) The protein level of CXCL10 in vivo. (G) The Luciferase assay showed the regulatory relationship between PTB and CXCL10. *P < 0:05, **P < 0:01, ***P < 0:001, and ****P < 0:0001.

FIGURE 2 Immunochemistry for CD8, CXCL10 and CXCR3 in mice skins and Western blotting analysis of JAK/STAT pathway in HaCaT. (A) Detection of CD8, CXCL10 and CXCR3 through immunohistochemistry. Strong staining of CD8 was observed in the AAV-KRT14-Dcun1d1 group, but expression of CD8 was mild in the control and negative control groups. Compared with the other groups, CXCL10 staining was observed in dermal parts of skin biopsy sections from the AAV-KRT14-Dcun1d1 group. CXCR3 staining was close to the portal regions or blood vessels. The expression of CXCR3 was upregulated in the control and negative control groups. Red arrows indicate positive staining. A section of the image (magnification, ×100) in the upper column marked with the brown dotted frame is enlarged and displayed in the lower column. (B), Inhibition of DCUN1D1 by sgRNA was assessed by western blotting. (C), Expression levels of P-JAK1, P-JAK2, P-STAT1 and CXCL10 were assessed by Western blotting. (D–G), Statistical analysis. ns means no significant difference.

FIGURE 2 Immunochemistry for CD8, CXCL10 and CXCR3 in mice skins and Western blotting analysis of JAK/STAT pathway in HaCaT. (A) Detection of CD8, CXCL10 and CXCR3 through immunohistochemistry. Strong staining of CD8 was observed in the AAV-KRT14-Dcun1d1 group, but expression of CD8 was mild in the control and negative control groups. Compared with the other groups, CXCL10 staining was observed in dermal parts of skin biopsy sections from the AAV-KRT14-Dcun1d1 group. CXCR3 staining was close to the portal regions or blood vessels. The expression of CXCR3 was upregulated in the control and negative control groups. Red arrows indicate positive staining. A section of the image (magnification, ×100) in the upper column marked with the brown dotted frame is enlarged and displayed in the lower column. (B), Inhibition of DCUN1D1 by sgRNA was assessed by western blotting. (C), Expression levels of P-JAK1, P-JAK2, P-STAT1 and CXCL10 were assessed by Western blotting. (D–G), Statistical analysis. ns means no significant difference.

Fig. 3. Representative images of CXCL8 and CXCL10 inflammatory markers on B. burgdorferi-positive and negative breast cancer and normal breast tissues. Panels: B and C show B. burgdorferi-positive breast cancer tissues stained Borrelia monoclonal antibody (green) and CXCL8 monoclonal antibody (red). Panels: F and G show B. burgdorferi-positive breast cancer tissues stained Borrelia monoclonal antibody (green) and CXCL10 monoclonal antibody (red). Panels: D and H show no staining on B. burgdorferi-negative breast cancer tissue samples for both inflammatory markers, CXCL8 and CXCL10 respectively. Panels: A and E show negative control; normal breast tissues are negative for B. burgdorferi and both inflammatory markers. White scale bar: 100 µm