anti cc chemokine ligand 17 ccl17 antibody  (R&D Systems)

Journal: Cell Biology and Toxicology

Article Title: SENP3 mediated DeSUMOylation of macrophage derived CCL17 accelerates atherosclerosis via regulation of Treg

doi: 10.1007/s10565-025-10099-3

Figure Lengend Snippet: CCL17 was elevated in atherosclerotic model. The murine AS model was established by high-fat diet (HFD) to ApoE mice. A HE and Oil Red O analysis of aorta root tissues. B The levels of total cholesterol (TC), triglyceride (TG) and low-density lipoprotein cholesterol (LDL-C) in serum were measured by ELISA. C The ( C ) RNA levels of pro-inflammatory factors VCAM-1, MCP-1, TNF-α, IL-1β, and IL-6 was detected by qPCR assay. D Serum CCL17 level was detected by ELISA. E Immunofluorescence detection of co-localization of CCL17 and macrophages in plaque tissue of AS mice. F The level of CCL17 mRNA in mice plaque tissue was detected by qPCR. In vitro AS model was established by stimulating primary macrophage macrophages with ox-LDL. G The mRNA levels of inflammatory factors (IL-1β and IL-6) were detected by qPCR. H The level of CCL17 in cell supernatant was detected by ELISA. I The level of CCL17 in macrophages was detected by qPCR. * p < 0.05, *** p < 0.01, *** p < 0.001. N = 6

Article Snippet: Prior to the transwell migration assay, the induced Tregs were treated with recombinant mouse CCL17 (MCE, HY-P71891A) or recombinant mouse CCL22 (MCE, HY-P7248) or anti-CCL17 (R&D, Catalog #: MAB529) and anti-CCL22 antibodies (R&D, Catalog #: MAB529).

Techniques: Enzyme-linked Immunosorbent Assay, Immunofluorescence, In Vitro

Journal: Cell Biology and Toxicology

Article Title: SENP3 mediated DeSUMOylation of macrophage derived CCL17 accelerates atherosclerosis via regulation of Treg

doi: 10.1007/s10565-025-10099-3

Figure Lengend Snippet: Silencing CCL17 improves atherosclerosis in mice. After 4 weeks of AS modeling, sh-CCL17 encapsulated by AAV virus was injected into the tail vein of mice to knock down the expression of CCL17 in mice. A Western blot was used to detect the protein expression of CCL17 in mice plaque. B HE and oil red O staining were used to observe the pathological changes of arterial tissue in mice. C The levels of TC, TG and LDL-C in AS mice were measured by ELISA. D qPCR was used to detect the mRNA level of inflammatory factors (IL-1β, and IL-6). E The expression of lipid genes FASN, CD36, SCD1 and SREBP1 was detected by qPCR. * p < 0.05, *** p < 0.01, *** p < 0.001. N = 6

Article Snippet: Prior to the transwell migration assay, the induced Tregs were treated with recombinant mouse CCL17 (MCE, HY-P71891A) or recombinant mouse CCL22 (MCE, HY-P7248) or anti-CCL17 (R&D, Catalog #: MAB529) and anti-CCL22 antibodies (R&D, Catalog #: MAB529).

Techniques: Virus, Injection, Knockdown, Expressing, Western Blot, Staining, Enzyme-linked Immunosorbent Assay

Journal: Cell Biology and Toxicology

Article Title: SENP3 mediated DeSUMOylation of macrophage derived CCL17 accelerates atherosclerosis via regulation of Treg

doi: 10.1007/s10565-025-10099-3

Figure Lengend Snippet: Silencing CCL17 promotes the recruitment of Treg in AS plaque tissue. A The total CD4+ cells (CD3, CD4) in plaque tissue were detected by flow cytometry, and the proportion of cells in the upper right quadrant was counted. B The proportion of Treg cells (FOXP3, CD25) in CD4 cells was detected by flow cytometry. C The expression of FOXP3 in mouse plaque was detected by qPCR. D The expression of CD25 in mouse plaque was detected by immunofluorescence. * p <0.05, ** p <0.01, *** p <0.001. N =6

Article Snippet: Prior to the transwell migration assay, the induced Tregs were treated with recombinant mouse CCL17 (MCE, HY-P71891A) or recombinant mouse CCL22 (MCE, HY-P7248) or anti-CCL17 (R&D, Catalog #: MAB529) and anti-CCL22 antibodies (R&D, Catalog #: MAB529).

Techniques: Flow Cytometry, Expressing, Immunofluorescence

Journal: Cell Biology and Toxicology

Article Title: SENP3 mediated DeSUMOylation of macrophage derived CCL17 accelerates atherosclerosis via regulation of Treg

doi: 10.1007/s10565-025-10099-3

Figure Lengend Snippet: Macrophages stimulated by oxLDL affect the chemotaxis of Treg through CCL17 and CCL22 competition. Macrophages were stimulated with oxLDL, and Treg cells were co-cultured with macrophage supernatant. A Immunofluorescence detection of co-localization of CCL22 and macrophages (CD68) in plaque tissue of AS mice. B The content of CCL22 in the supernatant of macrophages was detected by ELISA. C Transwell detected the effect of macrophages on the chemotaxis of Treg. ( D - E ) Transwell detected the migration of Treg cells. * p < 0.05, ** p < 0.01, *** p < 0.001. N = 3

Article Snippet: Prior to the transwell migration assay, the induced Tregs were treated with recombinant mouse CCL17 (MCE, HY-P71891A) or recombinant mouse CCL22 (MCE, HY-P7248) or anti-CCL17 (R&D, Catalog #: MAB529) and anti-CCL22 antibodies (R&D, Catalog #: MAB529).

Techniques: Chemotaxis Assay, Cell Culture, Immunofluorescence, Enzyme-linked Immunosorbent Assay, Migration

Journal: Cell Biology and Toxicology

Article Title: SENP3 mediated DeSUMOylation of macrophage derived CCL17 accelerates atherosclerosis via regulation of Treg

doi: 10.1007/s10565-025-10099-3

Figure Lengend Snippet: The stability of CCL17 protein is regulated by SENP3-mediated de-SUMOylation. A Western blot detected the level of SENP3 in macrophages induced by oxLDL. B SENP3 was overexpressed in macrophages, and the expressions of SENP3 and CCL17 were detected by western blot. C Bioinformatics on-line prediction of sumoylation site of CCL17 protein. D IP detection of the effect of SENP3 on the DeSUMOylation of CCL17. E & ( F ) The effect of SENP3 on the stability of CCL17 protein was detected by CHX protein degradation experiment. G Co-IP experiment verified the binding relationship between SENP3 and CCL17. H The DeSUMOylation of mutant CCL17 of K115R was detected by IP. I The binding relationship between SENP3 and CCL17 was verified through GST Pull-down. * p < 0.05, ** p < 0.01, *** p < 0.001. N = 3

Article Snippet: Prior to the transwell migration assay, the induced Tregs were treated with recombinant mouse CCL17 (MCE, HY-P71891A) or recombinant mouse CCL22 (MCE, HY-P7248) or anti-CCL17 (R&D, Catalog #: MAB529) and anti-CCL22 antibodies (R&D, Catalog #: MAB529).

Techniques: Western Blot, Co-Immunoprecipitation Assay, Binding Assay, Mutagenesis

Journal: Cell Biology and Toxicology

Article Title: SENP3 mediated DeSUMOylation of macrophage derived CCL17 accelerates atherosclerosis via regulation of Treg

doi: 10.1007/s10565-025-10099-3

Figure Lengend Snippet: Knocking down SENP3 improved the progress of AS. After 4 weeks of AS modeling, sh-SENP3 encapsulated by AAV virus was injected into the tail vein of mice to knock down the level of SENP3 in mice. A Western blot detected the expression of SENP3 in mice plaque tissue. B HE staining and oil red O staining were used to observe the pathological changes of arterial tissue in mice. C The contents of TC, TG and LDL-C in mice were detected by ELISA. D The levels of inflammatory factors in mice were detected by ELISA. E qPCR detected the expression level of lipid-related genes. F Flow detection of Treg cells in mice plaque tissue. G The co-localization of CCL17/CD68 in mice plaque tissues was detected by immunofluorescence. H The level of CD25 in the mice plaque was detected by immunofluorescence. * p < 0.05, ** p < 0.01, *** p < 0.001. N = 6

Article Snippet: Prior to the transwell migration assay, the induced Tregs were treated with recombinant mouse CCL17 (MCE, HY-P71891A) or recombinant mouse CCL22 (MCE, HY-P7248) or anti-CCL17 (R&D, Catalog #: MAB529) and anti-CCL22 antibodies (R&D, Catalog #: MAB529).

Techniques: Virus, Injection, Knockdown, Western Blot, Expressing, Staining, Enzyme-linked Immunosorbent Assay, Immunofluorescence

Journal: Cell Biology and Toxicology

Article Title: SENP3 mediated DeSUMOylation of macrophage derived CCL17 accelerates atherosclerosis via regulation of Treg

doi: 10.1007/s10565-025-10099-3

Figure Lengend Snippet: SENP3-mediated regulation of CCL17 in atherosclerosis. In atherosclerosis, SENP3 levels are elevated in macrophages, where it mediates the DeSUMOylation of CCL17, stabilizing its protein levels. Increased CCL17 secretion subsequently competitively inhibits Treg cell recruitment, exacerbating atherosclerosis progression

Article Snippet: Prior to the transwell migration assay, the induced Tregs were treated with recombinant mouse CCL17 (MCE, HY-P71891A) or recombinant mouse CCL22 (MCE, HY-P7248) or anti-CCL17 (R&D, Catalog #: MAB529) and anti-CCL22 antibodies (R&D, Catalog #: MAB529).

Techniques:

Journal: Experimental & Molecular Medicine

Article Title: H3K18 lactylation in cancer-associated fibroblasts drives malignant pleural effusion progression via TNFR2 + T reg recruitment

doi: 10.1038/s12276-025-01557-3

Figure Lengend Snippet: a KEGG pathway enrichment of DEGs between FACS-sorted TNFR2 + and TNFR2 − CD4 + T cells from MPE ( n = 3). b , c Volcano plot ( b ) and heatmap ( c ) of DEGs related to the chemokine signaling pathway. d , e Flow cytometry histograms ( d ) and comparisons of chemokine receptor expression (CXCR6, CCR4 and CCR6) ( e ) on TNFR2 + T reg cells and TNFR2 − T reg cells ( n = 13). f Schematic of Transwell chemotaxis assay testing TNFR2 − T reg chemotaxis toward MPE supernatant (by Figdraw). g , h Transwell chemotaxis assay comparing TNFR2 + T reg frequencies between freshly isolated cells and cells that migrated toward MPE supernatant after 4 h incubation. i Concentrations of CXCL16, CCL17, CCL22 and CCL20 in MPE and PB were quantified using ELISA ( n = 16). j Schematic of chemotaxis assay to investigate the chemotatic axis to attract TNFR2 + T reg cells in MPE. k , l Flow cytometry histograms and comparisons of chemotaxis of TNFR2 + T reg cells in response to MPE in the presence of anti-CXCL16, anti-CCL17, anti-CCL22 or anti-CCL20 mAbs. Data shown in d , e , g – i , k and l are representative of at least three independent experiments (mean ± s.d.). Statistical analysis was performed using paired two-tailed Student’s t -test ( e and h ), Wilcoxon test ( i ) or one-way ANOVA ( l ). * P < 0.05, ** P < 0.01, **** P < 0.0001. ns not significant, mAbs monoclonal antibodies.

Article Snippet: In specific experimental conditions, the following reagents were added to the lower chamber: anti-CCL17 antibody (50 ng/ml, #MAB364-SP, R&D Systems), anti-CCL20 antibody (50 ng/ml, #MAB360-SP, R&D Systems), anti-CCL22 antibody (50 ng/ml, #MAB336-SP, R&D Systems), anti-CXCL16 antibody (50 ng/ml, #MAB976, R&D Systems) or recombinant human CXCL16 (100 ng/ml, #976-CX-025/CF, R&D Systems).

Techniques: Flow Cytometry, Expressing, Chemotaxis Assay, Isolation, Incubation, Enzyme-linked Immunosorbent Assay, Two Tailed Test, Bioprocessing