Journal: iScience

Article Title: M2 type tumor-associated macrophage-derived CCL-18 promotes glioma cell proliferation but does not mediates glioma recurrence after radiotherapy

doi: 10.1016/j.isci.2026.117695

Figure Lengend Snippet: CCL-18 may be the candidate-mediator of glioma recurrence (A) KEGG enrichment analysis of the 201 DEGs showing that the cytokine-cytokine receptor interaction pathway was the most significantly enriched. (B) Among cytokine-cytokine receptor interaction pathway, CCL-18 was the top one up-regulated DEG. Data were presented as average TPM. (C) Representative IHC staining of CCL-18 in primary and recurrent glioma samples from irradiated patients versus unirradiated patients. Scale bars: 200 μm and 100 μm (enlarged graph). (D and E) Quantification of IHC results in (C). The percent of CCL-18 positive cells in primary and recurrent glioma samples accepting radiotherapy (D), and without radiotherapy (E). Data were presented as paired individual value (two-tailed paired t test, ∗ p < 0.05). (F) The correlation between tumor volume doubling time and the level of CCL-18. Data were presented as Pearson correlation coefficient. (G) Kaplan-Meier curves showing the progression free survival probability of glioma patients accepting radiotherapy based on different expression levels of CCL-18. Data were presented as median ± 95% confidence intervals (∗∗ p < 0.01). Data were obtained from 15 paired primary glioma and recurrent glioma with radiotherapy, and 8 paired primary glioma and recurrent glioma without radiotherapy (C–G).

Article Snippet: recombinant CCL-18 , Med Chem Express , HY-P7265.

Techniques: Analysis, Immunohistochemistry, Irradiation, Two Tailed Test, Expressing

Journal: iScience

Article Title: M2 type tumor-associated macrophage-derived CCL-18 promotes glioma cell proliferation but does not mediates glioma recurrence after radiotherapy

doi: 10.1016/j.isci.2026.117695

Figure Lengend Snippet: Multivariate Cox regression analysis from TCGA

Article Snippet: recombinant CCL-18 , Med Chem Express , HY-P7265.

Techniques: Analysis, Expressing

Journal: iScience

Article Title: M2 type tumor-associated macrophage-derived CCL-18 promotes glioma cell proliferation but does not mediates glioma recurrence after radiotherapy

doi: 10.1016/j.isci.2026.117695

Figure Lengend Snippet: Radiation promotes macrophage to polarize into M2-TAMs, accompanying CCL-18 secretion (A) The mRNA level of CD163 and IL-10 after treatment with PMA or PMA+IL-4/13 on THP-1 cells. Data were presented as mean ± SEM (unpaired t test, ∗∗ p < 0.01, ∗∗∗ p < 0.001). (B) Representative immunoblot of CD163 and CD68 after PMA or PMA+IL-4/13 treatment in THP-1 cells. (C) Representative immunoblot of CD163 and CD68 after PMA treatment with or without different radiation doses. (D) The mRNA level of CD163 and IL-10 following the indicated treatment at different durations. Data were presented as mean ± SEM (one-way ANOVA, in CD163: F = 1.22, p = 0.32, ∗∗∗ p < 0.001; in IL-10: F = 1.82, p = 0.14, ∗∗∗ p < 0.001). (E) Representative immunoblot of CD163 and CD68 following the indicated treatment. (F) Representative immunofluorescence images of CD163 and CD68 staining following the indicated treatment. Scale bars: 200 μm. (G and H) Quantitative results of relative mean density of CD163 (G) and CD68 (H). Data were presented as mean ± SEM (one-way ANOVA, in CD163: F = 1.36, p = 0.3, ∗∗ p < 0.01, ∗∗∗ p < 0.001; in CD68: F = 1.54, p = 0.26, ∗ p < 0.05, ∗∗ p < 0.01). (I) Representative immunoblot of indicated antibodies on THP-1 cells after PMA treatment with or without radiation. (J and K) The mRNA level (J) and the protein abundance (K) of CCL-18 following the indicated treatment. Data were presented as mean ± SEM (one-way ANOVA, in mRNA: F = 1.35, p = 0.27, ∗∗ p < 0.01, ∗∗∗ p < 0.001; in protein: F = 3, p = 0.04, ∗∗∗ p < 0.001). Data were obtained from 4 independent experiments (A, F–H, and K), 3 independent experiments (B, C, E, and I) and 6 independent experiments (D and J).

Article Snippet: recombinant CCL-18 , Med Chem Express , HY-P7265.

Techniques: Western Blot, Immunofluorescence, Staining, Quantitative Proteomics

Journal: iScience

Article Title: M2 type tumor-associated macrophage-derived CCL-18 promotes glioma cell proliferation but does not mediates glioma recurrence after radiotherapy

doi: 10.1016/j.isci.2026.117695

Figure Lengend Snippet: CCL-18 does not mediate glioma cell proliferation following radiotherapy in vitro (A) Viability of GBM cells after treatment with different concentrations of CCL-18. Data were presented as mean ± SEM (one-way ANOVA, F = 1.9, p = 0.21, ∗∗ p < 0.01, ∗∗∗ p < 0.001). (B) Representative images of colony formation assay after CCL-18 (100 ng/mL) treatment. (C) Quantitative results from (B). Data were presented as mean ± SD (unpaired t test, ∗∗∗ p < 0.001). (D) Schematic workflow for the co-culture experiment. (E) Representative images of colony formation assay. (F) Quantitative results from (E). Data were presented as mean ± SD (unpaired t test, ∗ p < 0.05). (G) The mRNA level of PITPNM3, GPR30, and CCR8 on irradiated GBM cells. Data were presented as mean ± SEM (unpaired t test, ∗∗∗ p < 0.001). (H) Representative immunoblot of PITPNM3, GPR30, and CCR8 on irradiated GBM cells. (I) Quantitative results from (H). Data were presented as mean ± SEM (unpaired t test, ∗ p < 0.05, ∗∗ p < 0.01). (J) Immunoblot of CCR8 after overexpression. (K) Representative images of colony formation assay on irradiated GBM cells after CCL-18 (100 ng/mL) treatment. (L) Quantitative results from (K). Data were presented as mean ± SD (two-way ANOVA, F = 4.9, p = 0.06, ∗ p < 0.05, ∗∗ p < 0.01). Data were obtained from 3 independent experiments (A–L).

Article Snippet: recombinant CCL-18 , Med Chem Express , HY-P7265.

Techniques: In Vitro, Colony Assay, Co-culture Assay, Irradiation, Western Blot, Over Expression

Journal: iScience

Article Title: M2 type tumor-associated macrophage-derived CCL-18 promotes glioma cell proliferation but does not mediates glioma recurrence after radiotherapy

doi: 10.1016/j.isci.2026.117695

Figure Lengend Snippet: CCL-18 do not mediate glioma recurrence following radiotherapy in vivo (A) Viability of GL261 cells after treatment with different concentrations of CCL-18. Data were presented as mean ± SEM (one-way ANOVA, F = 0.9, p = 0.48, ∗∗∗ p < 0.001). (B) Viability of GL261 cells after treatment with CCL-18 (100 ng/mL) and R243 (50, 100 μM). Data were presented as mean ± SEM (one-way ANOVA, F = 1.43, p = 0.28, ∗ p < 0.05, ∗∗∗ p < 0.001). (C) Representative immunoblot of ACP5, Akt, and phosphorylated Akt on GL261 cells after CCL-18 (100 ng/mL) treatment. (D) Schematic workflow for the cell-derived allograft experiment. (E) The bioluminescence value in mice receiving radiation on the indicated days. Data were presented as mean ± SEM (one-way ANOVA, in radiation: F = 2.48, p = 0.1, ∗ p < 0.05; in radiation with CCL-18 treatment: F = 1.41, p = 0.3, ∗ p < 0.05). (F) Representative pseudo-color bioluminescence images of intracranial allografts receiving radiation with or without CCL-18 administration. (G) Quantitative results from (F) on the indicated days. Data were presented as mean ± SEM (two-way ANOVA, F = 2.39, p = 0.04, ∗ p < 0.05, ∗∗ p < 0.01). (H) Kaplan-Meier curve showing the percent survival of mice receiving different treatment. Data were presented as median (∗∗∗ p < 0.001). (I) The percent of M1-TAM in glioma after radiation with or without CCL-18 treatment. (J) Quantitative results from (I). Data were presented as mean ± SD (one-way ANOVA, F = 1.46, p = 0.26). (K)The percent of M2-TAM in glioma after radiation with or without CCL-18 treatment. (L) Quantitative results from (K). Data were presented as mean ± SD (one-way ANOVA, F = 0.1, p = 0.9). Data were obtained from 3 independent experiments (A, C, and I–L), and 4 independent experiments (B). Data were obtained from ≥6 mice (E), ≥11 mice (G and H), and 3 mice (I–L).

Article Snippet: recombinant CCL-18 , Med Chem Express , HY-P7265.

Techniques: In Vivo, Western Blot, Derivative Assay

Journal: iScience

Article Title: M2 type tumor-associated macrophage-derived CCL-18 promotes glioma cell proliferation but does not mediates glioma recurrence after radiotherapy

doi: 10.1016/j.isci.2026.117695

Figure Lengend Snippet:

Article Snippet: recombinant CCL-18 , Med Chem Express , HY-P7265.

Techniques: Cell-Signaling, Virus, Tissue, Microarray, Recombinant, cDNA Synthesis, Enzyme-linked Immunosorbent Assay, Software, Biomarker Discovery, In Vivo Imaging

Journal: iScience

Article Title: M2 type tumor-associated macrophage-derived CCL-18 promotes glioma cell proliferation but does not mediates glioma recurrence after radiotherapy

doi: 10.1016/j.isci.2026.117695

Figure Lengend Snippet: CCL-18 may be the candidate-mediator of glioma recurrence (A) KEGG enrichment analysis of the 201 DEGs showing that the cytokine-cytokine receptor interaction pathway was the most significantly enriched. (B) Among cytokine-cytokine receptor interaction pathway, CCL-18 was the top one up-regulated DEG. Data were presented as average TPM. (C) Representative IHC staining of CCL-18 in primary and recurrent glioma samples from irradiated patients versus unirradiated patients. Scale bars: 200 μm and 100 μm (enlarged graph). (D and E) Quantification of IHC results in (C). The percent of CCL-18 positive cells in primary and recurrent glioma samples accepting radiotherapy (D), and without radiotherapy (E). Data were presented as paired individual value (two-tailed paired t test, ∗ p < 0.05). (F) The correlation between tumor volume doubling time and the level of CCL-18. Data were presented as Pearson correlation coefficient. (G) Kaplan-Meier curves showing the progression free survival probability of glioma patients accepting radiotherapy based on different expression levels of CCL-18. Data were presented as median ± 95% confidence intervals (∗∗ p < 0.01). Data were obtained from 15 paired primary glioma and recurrent glioma with radiotherapy, and 8 paired primary glioma and recurrent glioma without radiotherapy (C–G).

Article Snippet: CCL-18 ELISA kit , Boster Biological Technology , EK0686.

Techniques: Analysis, Immunohistochemistry, Irradiation, Two Tailed Test, Expressing

Journal: iScience

Article Title: M2 type tumor-associated macrophage-derived CCL-18 promotes glioma cell proliferation but does not mediates glioma recurrence after radiotherapy

doi: 10.1016/j.isci.2026.117695

Figure Lengend Snippet: Multivariate Cox regression analysis from TCGA

Article Snippet: CCL-18 ELISA kit , Boster Biological Technology , EK0686.

Techniques: Analysis, Expressing

Journal: iScience

Article Title: M2 type tumor-associated macrophage-derived CCL-18 promotes glioma cell proliferation but does not mediates glioma recurrence after radiotherapy

doi: 10.1016/j.isci.2026.117695

Figure Lengend Snippet: Radiation promotes macrophage to polarize into M2-TAMs, accompanying CCL-18 secretion (A) The mRNA level of CD163 and IL-10 after treatment with PMA or PMA+IL-4/13 on THP-1 cells. Data were presented as mean ± SEM (unpaired t test, ∗∗ p < 0.01, ∗∗∗ p < 0.001). (B) Representative immunoblot of CD163 and CD68 after PMA or PMA+IL-4/13 treatment in THP-1 cells. (C) Representative immunoblot of CD163 and CD68 after PMA treatment with or without different radiation doses. (D) The mRNA level of CD163 and IL-10 following the indicated treatment at different durations. Data were presented as mean ± SEM (one-way ANOVA, in CD163: F = 1.22, p = 0.32, ∗∗∗ p < 0.001; in IL-10: F = 1.82, p = 0.14, ∗∗∗ p < 0.001). (E) Representative immunoblot of CD163 and CD68 following the indicated treatment. (F) Representative immunofluorescence images of CD163 and CD68 staining following the indicated treatment. Scale bars: 200 μm. (G and H) Quantitative results of relative mean density of CD163 (G) and CD68 (H). Data were presented as mean ± SEM (one-way ANOVA, in CD163: F = 1.36, p = 0.3, ∗∗ p < 0.01, ∗∗∗ p < 0.001; in CD68: F = 1.54, p = 0.26, ∗ p < 0.05, ∗∗ p < 0.01). (I) Representative immunoblot of indicated antibodies on THP-1 cells after PMA treatment with or without radiation. (J and K) The mRNA level (J) and the protein abundance (K) of CCL-18 following the indicated treatment. Data were presented as mean ± SEM (one-way ANOVA, in mRNA: F = 1.35, p = 0.27, ∗∗ p < 0.01, ∗∗∗ p < 0.001; in protein: F = 3, p = 0.04, ∗∗∗ p < 0.001). Data were obtained from 4 independent experiments (A, F–H, and K), 3 independent experiments (B, C, E, and I) and 6 independent experiments (D and J).

Article Snippet: CCL-18 ELISA kit , Boster Biological Technology , EK0686.

Techniques: Western Blot, Immunofluorescence, Staining, Quantitative Proteomics

Journal: iScience

Article Title: M2 type tumor-associated macrophage-derived CCL-18 promotes glioma cell proliferation but does not mediates glioma recurrence after radiotherapy

doi: 10.1016/j.isci.2026.117695

Figure Lengend Snippet: CCL-18 does not mediate glioma cell proliferation following radiotherapy in vitro (A) Viability of GBM cells after treatment with different concentrations of CCL-18. Data were presented as mean ± SEM (one-way ANOVA, F = 1.9, p = 0.21, ∗∗ p < 0.01, ∗∗∗ p < 0.001). (B) Representative images of colony formation assay after CCL-18 (100 ng/mL) treatment. (C) Quantitative results from (B). Data were presented as mean ± SD (unpaired t test, ∗∗∗ p < 0.001). (D) Schematic workflow for the co-culture experiment. (E) Representative images of colony formation assay. (F) Quantitative results from (E). Data were presented as mean ± SD (unpaired t test, ∗ p < 0.05). (G) The mRNA level of PITPNM3, GPR30, and CCR8 on irradiated GBM cells. Data were presented as mean ± SEM (unpaired t test, ∗∗∗ p < 0.001). (H) Representative immunoblot of PITPNM3, GPR30, and CCR8 on irradiated GBM cells. (I) Quantitative results from (H). Data were presented as mean ± SEM (unpaired t test, ∗ p < 0.05, ∗∗ p < 0.01). (J) Immunoblot of CCR8 after overexpression. (K) Representative images of colony formation assay on irradiated GBM cells after CCL-18 (100 ng/mL) treatment. (L) Quantitative results from (K). Data were presented as mean ± SD (two-way ANOVA, F = 4.9, p = 0.06, ∗ p < 0.05, ∗∗ p < 0.01). Data were obtained from 3 independent experiments (A–L).

Article Snippet: CCL-18 ELISA kit , Boster Biological Technology , EK0686.

Techniques: In Vitro, Colony Assay, Co-culture Assay, Irradiation, Western Blot, Over Expression

Journal: iScience

Article Title: M2 type tumor-associated macrophage-derived CCL-18 promotes glioma cell proliferation but does not mediates glioma recurrence after radiotherapy

doi: 10.1016/j.isci.2026.117695

Figure Lengend Snippet: CCL-18 do not mediate glioma recurrence following radiotherapy in vivo (A) Viability of GL261 cells after treatment with different concentrations of CCL-18. Data were presented as mean ± SEM (one-way ANOVA, F = 0.9, p = 0.48, ∗∗∗ p < 0.001). (B) Viability of GL261 cells after treatment with CCL-18 (100 ng/mL) and R243 (50, 100 μM). Data were presented as mean ± SEM (one-way ANOVA, F = 1.43, p = 0.28, ∗ p < 0.05, ∗∗∗ p < 0.001). (C) Representative immunoblot of ACP5, Akt, and phosphorylated Akt on GL261 cells after CCL-18 (100 ng/mL) treatment. (D) Schematic workflow for the cell-derived allograft experiment. (E) The bioluminescence value in mice receiving radiation on the indicated days. Data were presented as mean ± SEM (one-way ANOVA, in radiation: F = 2.48, p = 0.1, ∗ p < 0.05; in radiation with CCL-18 treatment: F = 1.41, p = 0.3, ∗ p < 0.05). (F) Representative pseudo-color bioluminescence images of intracranial allografts receiving radiation with or without CCL-18 administration. (G) Quantitative results from (F) on the indicated days. Data were presented as mean ± SEM (two-way ANOVA, F = 2.39, p = 0.04, ∗ p < 0.05, ∗∗ p < 0.01). (H) Kaplan-Meier curve showing the percent survival of mice receiving different treatment. Data were presented as median (∗∗∗ p < 0.001). (I) The percent of M1-TAM in glioma after radiation with or without CCL-18 treatment. (J) Quantitative results from (I). Data were presented as mean ± SD (one-way ANOVA, F = 1.46, p = 0.26). (K)The percent of M2-TAM in glioma after radiation with or without CCL-18 treatment. (L) Quantitative results from (K). Data were presented as mean ± SD (one-way ANOVA, F = 0.1, p = 0.9). Data were obtained from 3 independent experiments (A, C, and I–L), and 4 independent experiments (B). Data were obtained from ≥6 mice (E), ≥11 mice (G and H), and 3 mice (I–L).

Article Snippet: CCL-18 ELISA kit , Boster Biological Technology , EK0686.

Techniques: In Vivo, Western Blot, Derivative Assay

Journal: iScience

Article Title: M2 type tumor-associated macrophage-derived CCL-18 promotes glioma cell proliferation but does not mediates glioma recurrence after radiotherapy

doi: 10.1016/j.isci.2026.117695

Figure Lengend Snippet:

Article Snippet: CCL-18 ELISA kit , Boster Biological Technology , EK0686.

Techniques: Cell-Signaling, Virus, Tissue, Microarray, Recombinant, cDNA Synthesis, Enzyme-linked Immunosorbent Assay, Software, Biomarker Discovery, In Vivo Imaging

Journal: bioRxiv

Article Title: Combined antagonism of Oncostatin M (OSM) and Interleukin 6 (IL-6) provides both anti-fibrotic and anti-inflammatory benefit in pulmonary fibrosis

doi: 10.64898/2025.12.25.695625

Figure Lengend Snippet: a. Alveolar macrophages (CD45 + CD11c + SigF + ) and CD64 + (CD45 + CD11c + SigF − MHCII + CD11b + CD64 + ) macrophages were FACS sorted from the lungs of WT mice 5 and 14 days post BLM treatment. Sorted cells were then placed in culture for 24 hours and CCL2, CCL3 and CCL4 was analyzed using Luminex. Graphs show mean of two independent experiments ± SD. * P<0.05. b. WT BMDMs were treated with IL-4 and IL-13 +/− IL-6 for 24 hours before gene expression analysis was assessed by qRT-PCR (n=6). Graphs show mean ± SD. * P<0.05. c. WT BMDMs were treated with IFNã and LPS +/− IL-6 for 24 hours before gene expression analysis was assessed by qRT-PCR (n=6). Graphs show mean ± SD. * P<0.05. d. WT BMDMs were treated with IL-4 and IL-13 +/− IL-6 for 24 hours with CCL2 measured in supernatant by Luminex and gene expression assessed by qRT-PCR (n=6). Graphs show mean ± SD. * P<0.05. e. WT BMDMs were treated with IL-4 and IL-13 +/− IL-6 for 24 hours before RNA was extracted for RNA-sequencing. Heat map showing the most differentially upregulated genes between untreated and IL-4 + IL-13 +IL-6 treatment across all treatment groups (top 40 by fold change and adjusted P value <0.05, n=3). f. Monocyte derived macrophages (MDMs) were generated from healthy donors and polarized with IL-4 and IL-13 +/− IL-6 for 24 hours. CCL18 mRNA and protein was measured using qRT-PCR and ELISA, respectively (n=7). Graphs show mean ± SD. * P<0.05. g. Monocyte derived macrophages (MDMs) were generated from healthy donors and polarized with IL-4 and IL-13 +/− IL-6 for 24 hours. RNA was extracted for RNA sequencing. Heatmap showing the most differentially upregulated genes are between untreated and IL-4 + IL-13 +IL-6 treatment across all treatment groups (top 40 by fold change, adjusted p<0.05, n=3).

Article Snippet: Ccl2 (Mm00441242_m1), Ccr2 (Mm99999051_gH), Cd64 (Mm00438874), Col1a1 (Mm00801666_g1), Col1a2 (Mm00483888_m1), Fn1 (Mm01256744_m1), Tgfb1 (Mm01178820_m1), Arg1 (Mm00475988_m1), Cd206 (Mm01329362_m1), Nos2 (Mm00440502) and CCL18 (Hs00268113_m1).

Techniques: Luminex, Gene Expression, Quantitative RT-PCR, RNA Sequencing, Derivative Assay, Generated, Enzyme-linked Immunosorbent Assay

Journal: bioRxiv

Article Title: Combined antagonism of Oncostatin M (OSM) and Interleukin 6 (IL-6) provides both anti-fibrotic and anti-inflammatory benefit in pulmonary fibrosis

doi: 10.64898/2025.12.25.695625

Figure Lengend Snippet: a. Lung biopsies were obtained from healthy controls (n=9) and IPF patients (n=24), RNA-seq was carried out and FCGR1A (CD64), CCL2 and CCL18 transcripts analyzed. Graphs show normalized log2 CPM, mean ± SD. ***P<0.0005, NS not significant. b. Skin biopsies obtained from healthy controls (n=14) and SSc patients (n=36) participating in the focuSSced clinical trial and FCGR1A (CD64), CCL2 and CCL18 transcripts measured at baseline. Graphs show normalized log2 CPM, mean ± SD. * P<0.05, ***P<0.0005, NS not significant. c. Serum was obtained from SSc patients (n=207) participating in the focuSSced clinical trial and serum CCL18 was measured at baseline and after 24 or 48 weeks of PBO (n=104) or TCZ (n=103) treatment. P values calculated by ttests between baseline and week 48. Graphs show ng/mL and mean (bar). *** P<0.0005, NS not significant.

Article Snippet: Ccl2 (Mm00441242_m1), Ccr2 (Mm99999051_gH), Cd64 (Mm00438874), Col1a1 (Mm00801666_g1), Col1a2 (Mm00483888_m1), Fn1 (Mm01256744_m1), Tgfb1 (Mm01178820_m1), Arg1 (Mm00475988_m1), Cd206 (Mm01329362_m1), Nos2 (Mm00440502) and CCL18 (Hs00268113_m1).

Techniques: RNA Sequencing