Fig 2: IL-6 levels are higher in human lung adenocarcinoma tissues and corresponding TAM infiltration. (A) Representative immunohistochemistry images of IL-6 in lung adenocarcinoma tissues and matched normal lung tissues (magnification ×200). (B) Statistical analysis of the immunohistochemistry scores for the expression of IL-6 in 30 pairs of lung adenocarcinoma tissues and matched normal lung tissues, **P<0.01, compared with the matched normal lung tissue group. (C) Representative immunohistochemistry images with high and low levels of IL-6 and CD68 (magnification ×200). (D) Scatter chart showing a positive correlation between the expression levels of IL-6 and CD68 in 30 pairs of lung adenocarcinoma tissues. IL-6, interleukin-6; TAM, tumor-associated macrophage.

Fig 3: Quantitative comparison of the number of positive cells per field for (A) macrophages (CD68) and (B) T lymphocytes (CD5) showing significant differences for the BMSCs + ASC group compared with the ASC group (*P<0.05) and control group (#P<0.05) at 2 weeks after surgery. (C) IgM shows no significant difference (P>0.05) among the groups. ASC, acellular spinal cord; BMSCs, bone marrow stromal cells; IgM, immunoglobulin M.

Fig 4: AO dose-dependently suppressed the expression of T-helper (Th) cells, cytotoxic T cells, and the T-cell co-receptor and inhibited the expression of macrophage and MHC class II in asthma.AO (a) inhibited the expression of CD3+ T-cell co-receptors in a dose-dependent manner, (b) significantly suppressed the upregulation of CD4+ Th cells, (c) downregulated the expression of CD8+ cytotoxic T cells, and (d) decreased CD68+ macrophasges. (e) AO also inhibited the expression of MHC class II. Immunopositive cells were counted in five randomly selected non-overlapping fields (×200 magnification) of three separately immunostained lung sections per animal. A, vehicle control; B, asthma induction; C, dexamethasone; D, 25 mg/kg/day ACA; E 50 mg/kg/day ACA. CD3: T-cell co-receptor; CD4: Th cell; CD8: cytotoxic T cell; CD68: macrophage; MHC class II: major histocompatibility complex class II molecules. *p<0.05 vs. control; **p<0.001 vs. control; $ p<0.05 vs. asthma induction; $$ p<0.001 vs. asthma induction; # p<0.05 vs. dexamethasone; ## p<0.001 vs. dexamethasone; s p<0.05 vs. 50 mg/kg/day; ss p<0.001 vs. 50 mg/kg/day; p p<0.05 vs. 200 mg/kg/day; pp p<0.001 vs. 200 mg/kg/day; ¥ p<0.05 vs. 400 mg/kg/day; ¥¥ p<0.001 vs. 400 mg/kg/day.

Fig 5: Time-dependent response of glial cells to traumatic brain injury. (A) Western blot of the time course of expression changes in GFAP and CD68. (B, C) The bar graphs show relative intensities for GFAP and CD68. The results are shown as the mean ± SD. **p < 0.01 by one-way ANOVA. (D) Reactive astrocytes surround damaged regions while microglia populate the center of the damaged region at 3 dpi. (E) Quantitative analysis for distances of IBA1 + activated microglia, and GFAP + reactive astrocytes from the center of the lesion in (D) from 4 mice. *p < 0.05 by two-tailed Student’s t-test. (F) Western blot samples reflect the changes in expression of AXL and GAS6 after TBI. (G, H) Quantitative analyses of AXL and GAS6 bands. *p < 0.05, **p < 0.01 by one-way ANOVA. (I) Immunofluorescence staining of GFAP, IBA1, NeuN (green), and AXL (red) in the ipsilateral cortex at 3 dpi; the nuclei were stained by DAPI (blue). (J) Immunofluorescence staining of GFAP (green), and AXL (red) at different time points post injury; the nuclei were stained by DAPI (blue). (K) Quantification analysis of the reactive astrocytes which expressed AXL kinase (GFAP+ & AXL+) after TBI in (J). n = 3 per group. **p < 0.05 by two-tail Student’s t-test