CCL22 Antibody - #DF7781

FIGURE 6 │FKN is involved EMT and fibrosis via the Wnt/β-catenin pathway in the kidney of 760 MRL/lpr mice. Histopathological features of renal tissue in the MRL/lpr mice model were studied by 761 PASM staining (original magnification, ×400). (a) Control group; (b) IgG group; (c) rFKN group; (d) 762 anti-FKN group.

FIGURE 5 │12-week-old MRL/lpr mice were IP injected with isotype antibody, recombinant-FKN 749 protein, and anti-FKN antibody for 7 days. In kidney sections of MRL/lpr mice stained by IHC 750 (original magnification, ×400). (a) Control group; (b) IgG group; (c) rFKN group; (d) anti-FKN 751 group. (A1) Expression of FKN as examined by IHC staining in the renal tissues. (B1) Expression of 752 Wnt-4 as examined by IHC staining in the renal tissues. (C1) Expression of CCL22 as examined by 753 IHC staining in the renal tissues.

Figure 1. Transferrin is a potential contributory factor for intestinal tolerance dependent on gut microbiota. (A) Transferrin concentration in plasma of germ-free (GF) and specific pathogen-free (SPF) (control) mice determined by ELISA. Data represent means ± SD (n = 10), *p < 0.05, **p < 0.01 by one-way ANOVA with Dunnett’s post-hoc test. Western blotting (left) and quantification (right) analyses of transferrin levels in protein extracts from liver (B) and spleen (C) of SPF and GF mice. β-actin was used as the control. Data represent means ± SD (n = 10), *p < 0.05, **p < 0.01 by one-way ANOVA with Dunnett’s post-hoc test (B, C). (D-E) Transferrin, ALDH1A2, CCL22, TGF-β, and IL-10 levels in different gut tissue segments (duodenum, jejunum, ileum, caecum, and colon (D, J, I, C1, and C2)) of SPF (NC), GF (D), and broad-spectrum antibiotic (Abs)-treated SPF (E) mice were determined by Western blotting (left) and quantification (right) analyses. GAPDH was used as the control. Data represent means ± SD (n = 8),