Fig 2: Prognostic significance of CCL22 Expression in BC.Kaplan–Meier curves of overall survival (OS) (A) and progression-free survival (PFS) (B) for CCL22 expression in BC to show the association of CCL22 expression with reduced OS (P<0.0001) and PFS (P<0.0001). P values were calculated by the log-rank test.

Fig 3: M2‐TAMs promoted HCC progression. THP‐1 cells were incubated with 100 ng/mL PMA for 24 h to obtain M0 macrophages, and M0 macrophages were incubated with 20 ng/mL IL‐4 and IL‐13 to obtain M2‐TAMs. (A‐B) The levels of M2 markers (CD206, CD163 and CCL22) were detected by flow cytometry and western blot. (C) NEAT1 expression in M0 and M2‐TAMs was assessed by qRT‐PCR. We subsequently co‐treated HCC cells with M0‐TAMs and M2‐TAMs, and the HCC cells were cultured in ordinary culture medium as the control group. (D) CCK8 assay was performed to detect HCC cell viability. (E) Cell migration was examined by Transwell assays (Scale bars = 100 μm) (F) NEAT1 expression in HCC cells was detected by qRT‐PCR. The measurement data were presented as mean ± SD. All data was obtained from at least three replicate experiments. **p < 0.01, ***p < 0.001.

Fig 4: Anti-CCL22 antibody enhances the number of Tregs via the activation of STAT5 pathway. CD4+ T cells, isolated from RA, were treated with anti-CCL22 antibody (0.5 µg/ml) in the presence of STAT5 inhibitor (1 µM) or vehicle (DMSO) at 48 h, and then the number of Tregs (A) and protein levels of FOXP3, STAT5 and p-STAT5 (B) were assessed. GAPDH was used a loading control. **P<0.01 vs. control; ##P<0.01 vs. anti-CCL22. Tregs, regulatory T cells; STAT5, signal transducer and activator of transcription 5.

Fig 5: Roles of CCL22 in regulating the number and function associated makers of Tregs. (A and C) Stimulation of CD4+ T cells of RA patients with anti-CCL22 antibody (0.1, 0.2, 0.5, 1.0 and 2.0 µg/ml) caused apromoted effect on the number of Tregs, as well as a decrease of CCR4 while an increase in FOXP3 (C). (B and D) Stimulation of CD4+ T cells of HC with CCL22 protein (2, 10 and 50 ng/ml) caused inhibition of the number of Tregs (B), as well as increase in CCR4 while decreased FOXP3 (D). *P<0.05, **P<0.01 vs. control CD4+ T cells from RA; #P<0.05, ##P<0.01 vs. control CD4+ T cells from HC. Tregs, regulatory T cells; CCR4, C-C chemokine receptor 4.