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R&D Systems mouse ccl20 elisa

A Bulk sequencing data from TCGA (left) and GTEx (right) showing <t>CCL20</t> expression. Gastrointestinal tissues prominently express CCL20 while other epithelial tissues expressed little if any CCL20. B Expression of CCL20 by the different cell types found in primary tumors from a PDAC scRNA atlas . C CCL20 expression from a scRNA dataset healthy human colon (H) and colorectal cancer . D Expression of CCL20 by different cells found in a single nucleus RNA sequencing dataset of chronic pancreatitis biopsies . E CCR6, CCL20, IL-17A, and IL-23A in a scRNA datasets of CD45+ cells from human chronic pancreatitis or healthy patients . Pancreatitis was classified as hereditary if there were mutations present in PRSS1 gene. F Expression of CCL20 in a scRNA dataset of human ulcerative colitis (UC) and Crohn’s disease (CD) . G Differentially expressed chemokines found using MAST from a scRNA atlas of PDAC .

Mouse Ccl20 Elisa, supplied by R&D Systems, used in various techniques. Bioz Stars score: 92/100, based on 17 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/mouse+ccl20+elisa/bio_rxiv__64898__2026__04__13__717530-264-15-18?v=R%26D+Systems
Average 92 stars, based on 17 article reviews

mouse ccl20 elisa - by Bioz Stars, 2026-07

92/100 stars

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1) Product Images from "Mutant KRAS promotes NF-κB driven CCL20 chemokine expression in pancreatic ductal adenocarcinoma"

Article Title: Mutant KRAS promotes NF-κB driven CCL20 chemokine expression in pancreatic ductal adenocarcinoma

Journal: bioRxiv

doi: 10.64898/2026.04.13.717530

A Bulk sequencing data from TCGA (left) and GTEx (right) showing CCL20 expression. Gastrointestinal tissues prominently express CCL20 while other epithelial tissues expressed little if any CCL20. B Expression of CCL20 by the different cell types found in primary tumors from a PDAC scRNA atlas . C CCL20 expression from a scRNA dataset healthy human colon (H) and colorectal cancer . D Expression of CCL20 by different cells found in a single nucleus RNA sequencing dataset of chronic pancreatitis biopsies . E CCR6, CCL20, IL-17A, and IL-23A in a scRNA datasets of CD45+ cells from human chronic pancreatitis or healthy patients . Pancreatitis was classified as hereditary if there were mutations present in PRSS1 gene. F Expression of CCL20 in a scRNA dataset of human ulcerative colitis (UC) and Crohn’s disease (CD) . G Differentially expressed chemokines found using MAST from a scRNA atlas of PDAC .

Figure Legend Snippet: A Bulk sequencing data from TCGA (left) and GTEx (right) showing CCL20 expression. Gastrointestinal tissues prominently express CCL20 while other epithelial tissues expressed little if any CCL20. B Expression of CCL20 by the different cell types found in primary tumors from a PDAC scRNA atlas . C CCL20 expression from a scRNA dataset healthy human colon (H) and colorectal cancer . D Expression of CCL20 by different cells found in a single nucleus RNA sequencing dataset of chronic pancreatitis biopsies . E CCR6, CCL20, IL-17A, and IL-23A in a scRNA datasets of CD45+ cells from human chronic pancreatitis or healthy patients . Pancreatitis was classified as hereditary if there were mutations present in PRSS1 gene. F Expression of CCL20 in a scRNA dataset of human ulcerative colitis (UC) and Crohn’s disease (CD) . G Differentially expressed chemokines found using MAST from a scRNA atlas of PDAC .

Techniques Used: Sequencing, Expressing, RNA Sequencing

A Representative PCR analyses of CCL20 and CCR6 transcript expression across multiple human and B mouse PDAC cell lines. Data representative of 3 individual analyses. C Quantification of the CCL20 staining images. 3-7 fields of view were quantified per patient, with five patients per disease state . D Representative immunostaining for CCL20 (red) or DAPI-stained cell nuclei (blue) (top) with parallel sections stained with H&E (bottom) in both healthy human pancreas or E human PDAC samples. * denotes p ≤ 0.05, Student’s unpaired t-test. Size bar = 100 μm.

Figure Legend Snippet: A Representative PCR analyses of CCL20 and CCR6 transcript expression across multiple human and B mouse PDAC cell lines. Data representative of 3 individual analyses. C Quantification of the CCL20 staining images. 3-7 fields of view were quantified per patient, with five patients per disease state . D Representative immunostaining for CCL20 (red) or DAPI-stained cell nuclei (blue) (top) with parallel sections stained with H&E (bottom) in both healthy human pancreas or E human PDAC samples. * denotes p ≤ 0.05, Student’s unpaired t-test. Size bar = 100 μm.

Techniques Used: Expressing, Staining, Immunostaining

A Gene sets listed in Supplementary Data 7 were correlated with CCL20 expression in ductal cells from a scRNA dataset of human PDAC and B colorectal cancer . Values shown are Pearson’s correlation coefficients, all p values = 0. C TCGA PDAC patients and D colorectal cancer patients sorted by SBS1 (replicative age) signatures, with comparisons of their normalized CCL20 expression. E TCGA PDAC patients sorted by their CN1 (diploid) and F CN2 (tetraploid) signatures using data from previously reported . Similar analysis for colorectal cancer patients can be seen in G and H . I Normalized CCL20 methylation values (probe cg21643045) from all GI cancers (cancer types in the top row of ) sorted by CCL20 expression. J CCL20 high patients (relative to patients of same cancer type) with their CCL20 normalized methylation values plotted. Non-GI mucosal cancers are bladder, cervical, head and neck, both lung types, and both uterine tumor types. Panel C-I Student’s unpaired t -test was used with p values plotted. Panel J one-way ANOVA with Tukey’s test for multiple comparisons, * denotes p ≤ 0.05.

Figure Legend Snippet: A Gene sets listed in Supplementary Data 7 were correlated with CCL20 expression in ductal cells from a scRNA dataset of human PDAC and B colorectal cancer . Values shown are Pearson’s correlation coefficients, all p values = 0. C TCGA PDAC patients and D colorectal cancer patients sorted by SBS1 (replicative age) signatures, with comparisons of their normalized CCL20 expression. E TCGA PDAC patients sorted by their CN1 (diploid) and F CN2 (tetraploid) signatures using data from previously reported . Similar analysis for colorectal cancer patients can be seen in G and H . I Normalized CCL20 methylation values (probe cg21643045) from all GI cancers (cancer types in the top row of ) sorted by CCL20 expression. J CCL20 high patients (relative to patients of same cancer type) with their CCL20 normalized methylation values plotted. Non-GI mucosal cancers are bladder, cervical, head and neck, both lung types, and both uterine tumor types. Panel C-I Student’s unpaired t -test was used with p values plotted. Panel J one-way ANOVA with Tukey’s test for multiple comparisons, * denotes p ≤ 0.05.

Techniques Used: Expressing, Methylation

A The top three transcription factors inferred using CollecTRI from all pancreatic exocrine ductal cells in a single cell RNA dataset sorted by CCL20 expression. B Inferred transcription factors from tumor cells from a CRC dataset sorted by CCL20 expression. C qPCR and D ELISA for CCL20 transcript expression and protein secretion by human PANC-1 cell line. E qPCR for CXCL2 by the PANC-1 cell line. ND = not detected by qPCR. ns, not significant. F qPCR for CCL20 and G CXCL2 expression by the patient-derived 339 cell line possessing a KRAS G12V mutation. H qPCR and I ELISA for CCL20 in the murine KPC FC1242 stably expressing Firefly luciferase PDAC cell line. Treatments were for 24 hours. Concentrations of the individual treatments were: Erlotinib 500 nM, regorafenib 500 nM, MRTX1133 500 nM, gemcitabine 100 nM, TNF 20 ng/mL with 10 ng/mL of IL-1, and RMC-7977 300 nM. For resistant cell lines (denoted by -R), resistance was considered established when cells survived in full growth medium supplemented with 10 μM of the denoted chemotherapy drug. One-way ANOVA was used for statistical analysis with Dunnett’s test for multiple comparisons used to compare to the untreated cell line.

Figure Legend Snippet: A The top three transcription factors inferred using CollecTRI from all pancreatic exocrine ductal cells in a single cell RNA dataset sorted by CCL20 expression. B Inferred transcription factors from tumor cells from a CRC dataset sorted by CCL20 expression. C qPCR and D ELISA for CCL20 transcript expression and protein secretion by human PANC-1 cell line. E qPCR for CXCL2 by the PANC-1 cell line. ND = not detected by qPCR. ns, not significant. F qPCR for CCL20 and G CXCL2 expression by the patient-derived 339 cell line possessing a KRAS G12V mutation. H qPCR and I ELISA for CCL20 in the murine KPC FC1242 stably expressing Firefly luciferase PDAC cell line. Treatments were for 24 hours. Concentrations of the individual treatments were: Erlotinib 500 nM, regorafenib 500 nM, MRTX1133 500 nM, gemcitabine 100 nM, TNF 20 ng/mL with 10 ng/mL of IL-1, and RMC-7977 300 nM. For resistant cell lines (denoted by -R), resistance was considered established when cells survived in full growth medium supplemented with 10 μM of the denoted chemotherapy drug. One-way ANOVA was used for statistical analysis with Dunnett’s test for multiple comparisons used to compare to the untreated cell line.

Techniques Used: Single Cell, Expressing, Enzyme-linked Immunosorbent Assay, Derivative Assay, Mutagenesis, Stable Transfection, Luciferase

A Mean fluorescence intensity (MFI) of anti-phospho-p65-PE immunostained FC1245 and RMC-7977 (2 μM)-resistant FC1245 PDAC cells. * denotes p ≤ 0.05, Student’s unpaired t -test. B Expression of CCL20 in a single cell RNA dataset of pancreatic ductal cells obtained from mice with a Ptf1a specific tamoxifen inducible Kras -G12D. The time listed on the y-axis is time from when the initial tamoxifen was given. C The number of wild-type C57BL6 splenocytes migrated in a chemotaxis assay using conditioned media from the listed FC1242 PDAC cell line. The conditioned media was obtained from cells outlined in . One-way ANOVA was used for statistical analysis with Dunnett’s test for multiple comparisons used to compare to the untreated cell line D Treatment schema for mice treated implanted with orthotopic KPC1199 tumors and treated with either vehicle PBS or 100 μg CCL20LD. E The mass of the tumors from the experiment outlined in . F CD11c+ MHCII+ dendritic cells, G CD11b+ F4/80+ macrophages, and H MHCII high macrophages (as a percentage of macrophages) in the harvested tumors. * denotes p ≤ 0.05, Student’s unpaired t -test.

Figure Legend Snippet: A Mean fluorescence intensity (MFI) of anti-phospho-p65-PE immunostained FC1245 and RMC-7977 (2 μM)-resistant FC1245 PDAC cells. * denotes p ≤ 0.05, Student’s unpaired t -test. B Expression of CCL20 in a single cell RNA dataset of pancreatic ductal cells obtained from mice with a Ptf1a specific tamoxifen inducible Kras -G12D. The time listed on the y-axis is time from when the initial tamoxifen was given. C The number of wild-type C57BL6 splenocytes migrated in a chemotaxis assay using conditioned media from the listed FC1242 PDAC cell line. The conditioned media was obtained from cells outlined in . One-way ANOVA was used for statistical analysis with Dunnett’s test for multiple comparisons used to compare to the untreated cell line D Treatment schema for mice treated implanted with orthotopic KPC1199 tumors and treated with either vehicle PBS or 100 μg CCL20LD. E The mass of the tumors from the experiment outlined in . F CD11c+ MHCII+ dendritic cells, G CD11b+ F4/80+ macrophages, and H MHCII high macrophages (as a percentage of macrophages) in the harvested tumors. * denotes p ≤ 0.05, Student’s unpaired t -test.

Techniques Used: Fluorescence, Expressing, Single Cell, Chemotaxis Assay

A Graphical abstract summarizing the findings. CCL20 is not expressed in the healthy pancreas. In pancreatitis, it is expressed the lymphocytic infiltrate. In PanINs, CCL20 begins to be expressed by the ductal epithelium. In PDAC, CCL20 expression is further increased by the ductal tumor cells and infiltrating myeloid cells. CCL20 expression is lost with resistance to KRAS inhibitors, along with decreased phosphorylation of RELA , and is limited to the basal subtype. Inhibition of CCL20-CCR6 signaling increased levels of antigen presenting cells, including dendritic cells and MHCII-high macrophages within the tumor parenchyma.

Figure Legend Snippet: A Graphical abstract summarizing the findings. CCL20 is not expressed in the healthy pancreas. In pancreatitis, it is expressed the lymphocytic infiltrate. In PanINs, CCL20 begins to be expressed by the ductal epithelium. In PDAC, CCL20 expression is further increased by the ductal tumor cells and infiltrating myeloid cells. CCL20 expression is lost with resistance to KRAS inhibitors, along with decreased phosphorylation of RELA , and is limited to the basal subtype. Inhibition of CCL20-CCR6 signaling increased levels of antigen presenting cells, including dendritic cells and MHCII-high macrophages within the tumor parenchyma.

Techniques Used: Expressing, Phospho-proteomics, Inhibition

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Journal: bioRxiv

Article Title: Mutant KRAS promotes NF-κB driven CCL20 chemokine expression in pancreatic ductal adenocarcinoma

doi: 10.64898/2026.04.13.717530

Figure Lengend Snippet: A Bulk sequencing data from TCGA (left) and GTEx (right) showing CCL20 expression. Gastrointestinal tissues prominently express CCL20 while other epithelial tissues expressed little if any CCL20. B Expression of CCL20 by the different cell types found in primary tumors from a PDAC scRNA atlas . C CCL20 expression from a scRNA dataset healthy human colon (H) and colorectal cancer . D Expression of CCL20 by different cells found in a single nucleus RNA sequencing dataset of chronic pancreatitis biopsies . E CCR6, CCL20, IL-17A, and IL-23A in a scRNA datasets of CD45+ cells from human chronic pancreatitis or healthy patients . Pancreatitis was classified as hereditary if there were mutations present in PRSS1 gene. F Expression of CCL20 in a scRNA dataset of human ulcerative colitis (UC) and Crohn’s disease (CD) . G Differentially expressed chemokines found using MAST from a scRNA atlas of PDAC .

Article Snippet: The ELISAs were performed using the human CCL20 ELISA (R&D Systems, Minneapolis, MN, #DY360) or mouse CCL20 ELISA (R&D Systems #DY760) following the manufacturer’s protocol.

Techniques: Sequencing, Expressing, RNA Sequencing

Journal: bioRxiv

Article Title: Mutant KRAS promotes NF-κB driven CCL20 chemokine expression in pancreatic ductal adenocarcinoma

doi: 10.64898/2026.04.13.717530

Figure Lengend Snippet: A Representative PCR analyses of CCL20 and CCR6 transcript expression across multiple human and B mouse PDAC cell lines. Data representative of 3 individual analyses. C Quantification of the CCL20 staining images. 3-7 fields of view were quantified per patient, with five patients per disease state . D Representative immunostaining for CCL20 (red) or DAPI-stained cell nuclei (blue) (top) with parallel sections stained with H&E (bottom) in both healthy human pancreas or E human PDAC samples. * denotes p ≤ 0.05, Student’s unpaired t-test. Size bar = 100 μm.

Article Snippet: The ELISAs were performed using the human CCL20 ELISA (R&D Systems, Minneapolis, MN, #DY360) or mouse CCL20 ELISA (R&D Systems #DY760) following the manufacturer’s protocol.

Techniques: Expressing, Staining, Immunostaining

Journal: bioRxiv

Article Title: Mutant KRAS promotes NF-κB driven CCL20 chemokine expression in pancreatic ductal adenocarcinoma

doi: 10.64898/2026.04.13.717530

Figure Lengend Snippet: A Gene sets listed in Supplementary Data 7 were correlated with CCL20 expression in ductal cells from a scRNA dataset of human PDAC and B colorectal cancer . Values shown are Pearson’s correlation coefficients, all p values = 0. C TCGA PDAC patients and D colorectal cancer patients sorted by SBS1 (replicative age) signatures, with comparisons of their normalized CCL20 expression. E TCGA PDAC patients sorted by their CN1 (diploid) and F CN2 (tetraploid) signatures using data from previously reported . Similar analysis for colorectal cancer patients can be seen in G and H . I Normalized CCL20 methylation values (probe cg21643045) from all GI cancers (cancer types in the top row of ) sorted by CCL20 expression. J CCL20 high patients (relative to patients of same cancer type) with their CCL20 normalized methylation values plotted. Non-GI mucosal cancers are bladder, cervical, head and neck, both lung types, and both uterine tumor types. Panel C-I Student’s unpaired t -test was used with p values plotted. Panel J one-way ANOVA with Tukey’s test for multiple comparisons, * denotes p ≤ 0.05.

Article Snippet: The ELISAs were performed using the human CCL20 ELISA (R&D Systems, Minneapolis, MN, #DY360) or mouse CCL20 ELISA (R&D Systems #DY760) following the manufacturer’s protocol.

Techniques: Expressing, Methylation

Journal: bioRxiv

Article Title: Mutant KRAS promotes NF-κB driven CCL20 chemokine expression in pancreatic ductal adenocarcinoma

doi: 10.64898/2026.04.13.717530

Figure Lengend Snippet: A The top three transcription factors inferred using CollecTRI from all pancreatic exocrine ductal cells in a single cell RNA dataset sorted by CCL20 expression. B Inferred transcription factors from tumor cells from a CRC dataset sorted by CCL20 expression. C qPCR and D ELISA for CCL20 transcript expression and protein secretion by human PANC-1 cell line. E qPCR for CXCL2 by the PANC-1 cell line. ND = not detected by qPCR. ns, not significant. F qPCR for CCL20 and G CXCL2 expression by the patient-derived 339 cell line possessing a KRAS G12V mutation. H qPCR and I ELISA for CCL20 in the murine KPC FC1242 stably expressing Firefly luciferase PDAC cell line. Treatments were for 24 hours. Concentrations of the individual treatments were: Erlotinib 500 nM, regorafenib 500 nM, MRTX1133 500 nM, gemcitabine 100 nM, TNF 20 ng/mL with 10 ng/mL of IL-1, and RMC-7977 300 nM. For resistant cell lines (denoted by -R), resistance was considered established when cells survived in full growth medium supplemented with 10 μM of the denoted chemotherapy drug. One-way ANOVA was used for statistical analysis with Dunnett’s test for multiple comparisons used to compare to the untreated cell line.

Article Snippet: The ELISAs were performed using the human CCL20 ELISA (R&D Systems, Minneapolis, MN, #DY360) or mouse CCL20 ELISA (R&D Systems #DY760) following the manufacturer’s protocol.

Techniques: Single Cell, Expressing, Enzyme-linked Immunosorbent Assay, Derivative Assay, Mutagenesis, Stable Transfection, Luciferase

Journal: bioRxiv

Article Title: Mutant KRAS promotes NF-κB driven CCL20 chemokine expression in pancreatic ductal adenocarcinoma

doi: 10.64898/2026.04.13.717530

Figure Lengend Snippet: A Mean fluorescence intensity (MFI) of anti-phospho-p65-PE immunostained FC1245 and RMC-7977 (2 μM)-resistant FC1245 PDAC cells. * denotes p ≤ 0.05, Student’s unpaired t -test. B Expression of CCL20 in a single cell RNA dataset of pancreatic ductal cells obtained from mice with a Ptf1a specific tamoxifen inducible Kras -G12D. The time listed on the y-axis is time from when the initial tamoxifen was given. C The number of wild-type C57BL6 splenocytes migrated in a chemotaxis assay using conditioned media from the listed FC1242 PDAC cell line. The conditioned media was obtained from cells outlined in . One-way ANOVA was used for statistical analysis with Dunnett’s test for multiple comparisons used to compare to the untreated cell line D Treatment schema for mice treated implanted with orthotopic KPC1199 tumors and treated with either vehicle PBS or 100 μg CCL20LD. E The mass of the tumors from the experiment outlined in . F CD11c+ MHCII+ dendritic cells, G CD11b+ F4/80+ macrophages, and H MHCII high macrophages (as a percentage of macrophages) in the harvested tumors. * denotes p ≤ 0.05, Student’s unpaired t -test.

Article Snippet: The ELISAs were performed using the human CCL20 ELISA (R&D Systems, Minneapolis, MN, #DY360) or mouse CCL20 ELISA (R&D Systems #DY760) following the manufacturer’s protocol.

Techniques: Fluorescence, Expressing, Single Cell, Chemotaxis Assay

Journal: bioRxiv

Article Title: Mutant KRAS promotes NF-κB driven CCL20 chemokine expression in pancreatic ductal adenocarcinoma

doi: 10.64898/2026.04.13.717530

Figure Lengend Snippet: A Graphical abstract summarizing the findings. CCL20 is not expressed in the healthy pancreas. In pancreatitis, it is expressed the lymphocytic infiltrate. In PanINs, CCL20 begins to be expressed by the ductal epithelium. In PDAC, CCL20 expression is further increased by the ductal tumor cells and infiltrating myeloid cells. CCL20 expression is lost with resistance to KRAS inhibitors, along with decreased phosphorylation of RELA , and is limited to the basal subtype. Inhibition of CCL20-CCR6 signaling increased levels of antigen presenting cells, including dendritic cells and MHCII-high macrophages within the tumor parenchyma.

Article Snippet: The ELISAs were performed using the human CCL20 ELISA (R&D Systems, Minneapolis, MN, #DY360) or mouse CCL20 ELISA (R&D Systems #DY760) following the manufacturer’s protocol.

Techniques: Expressing, Phospho-proteomics, Inhibition

The increased levels of CCL20 in the prostate in experimental autoimmune prostatitis mice. (A) Immunohistochemical staining of CCL20 on paraffin‐embedded prostate sections. (B) Semi‐quantitative analysis of CCL20 in Immunohistochemical staining. (C) Relative expression of CCL20 and CCR6 in the prostate measured by RT‐qPCR. (D–F) The expression level of CCL20 and CCR6 in the prostate tissues assessed by Western Blot. (G, H) Quantitative analysis of CCL20 in the serum and prostate of mice determined by ELISA. Representative data from three independent experiments are shown. Data were presented as mean ± SD and were analysed using unpaired, two‐tailed Student's t‐test analysis. * p < 0.05; ** p < 0.01; *** p < 0.001.

Journal: Journal of Cellular and Molecular Medicine

Article Title: Unraveling CCL20's role by regulating Th17 cell chemotaxis in experimental autoimmune prostatitis

doi: 10.1111/jcmm.18445

Figure Lengend Snippet: The increased levels of CCL20 in the prostate in experimental autoimmune prostatitis mice. (A) Immunohistochemical staining of CCL20 on paraffin‐embedded prostate sections. (B) Semi‐quantitative analysis of CCL20 in Immunohistochemical staining. (C) Relative expression of CCL20 and CCR6 in the prostate measured by RT‐qPCR. (D–F) The expression level of CCL20 and CCR6 in the prostate tissues assessed by Western Blot. (G, H) Quantitative analysis of CCL20 in the serum and prostate of mice determined by ELISA. Representative data from three independent experiments are shown. Data were presented as mean ± SD and were analysed using unpaired, two‐tailed Student's t‐test analysis. * p < 0.05; ** p < 0.01; *** p < 0.001.

Article Snippet: The cytokines levels in serum of mice were measured by employing the Elisa kit for IL‐17A (Elabscience, E‐EL‐M0047c), IL‐17F (Multi‐Science, EK2196), IL‐22 (Elabscience, E‐EL‐M2446), IFN‐γ (Elabscience, E‐EL‐M0048), TNF‐α (Elabscience, E‐EL‐M3063), GM‐CSF (Elabscience, E‐MSEL‐M0022) and CCL20 (Elabscience, E‐EL‐M0013).

Techniques: Immunohistochemical staining, Staining, Expressing, Quantitative RT-PCR, Western Blot, Enzyme-linked Immunosorbent Assay, Two Tailed Test

The recruitment of Th17 cells by CCL20. (A, D) Counting Th17 cells chemoattracted by CCL20 through transwell assay. (B) Immunohistochemical staining of IL‐17A on paraffin‐embedded prostate sections in each group. (C) Assessment of cell viability of Th17 cells after treatment with rCCL20 or anti‐CCL20 neutralizing antibodies. (E) Semi‐quantitative analysis of CCL20 in Immunohistochemical staining. (F) Quantitative analysis of IL‐17A in the serum of mice determined by ELISA. (G, H) Flow cytometry analysis of CD4 + IL‐17A + cells in the prostate. (I–K) The expression level of IL‐17A and CCR6 in the prostate tissues determined by Western Blot. (L) Relative expression of IL‐17A and CCR6 in the prostate measured by RT‐qPCR. Representative data from three independent experiments are shown. (M, N) Quantitative analysis of inflammatory cytokines (IL‐17A, IL‐17F, IL‐22, IFN‐γ, TNF‐α, GM‐CSF) in the serum and prostate of mice determined by ELISA. Data were presented as mean ± SD and were analysed using one‐way anova analysis. ‘N.D.’ Not Determined; ‘ns’ p > 0.05; * p < 0.05; ** p < 0.01; *** p < 0.001.

Journal: Journal of Cellular and Molecular Medicine

Article Title: Unraveling CCL20's role by regulating Th17 cell chemotaxis in experimental autoimmune prostatitis

doi: 10.1111/jcmm.18445

Figure Lengend Snippet: The recruitment of Th17 cells by CCL20. (A, D) Counting Th17 cells chemoattracted by CCL20 through transwell assay. (B) Immunohistochemical staining of IL‐17A on paraffin‐embedded prostate sections in each group. (C) Assessment of cell viability of Th17 cells after treatment with rCCL20 or anti‐CCL20 neutralizing antibodies. (E) Semi‐quantitative analysis of CCL20 in Immunohistochemical staining. (F) Quantitative analysis of IL‐17A in the serum of mice determined by ELISA. (G, H) Flow cytometry analysis of CD4 + IL‐17A + cells in the prostate. (I–K) The expression level of IL‐17A and CCR6 in the prostate tissues determined by Western Blot. (L) Relative expression of IL‐17A and CCR6 in the prostate measured by RT‐qPCR. Representative data from three independent experiments are shown. (M, N) Quantitative analysis of inflammatory cytokines (IL‐17A, IL‐17F, IL‐22, IFN‐γ, TNF‐α, GM‐CSF) in the serum and prostate of mice determined by ELISA. Data were presented as mean ± SD and were analysed using one‐way anova analysis. ‘N.D.’ Not Determined; ‘ns’ p > 0.05; * p < 0.05; ** p < 0.01; *** p < 0.001.

Techniques: Transwell Assay, Immunohistochemical staining, Staining, Enzyme-linked Immunosorbent Assay, Flow Cytometry, Expressing, Western Blot, Quantitative RT-PCR

The potential source CCL20 in the prostate of experimental autoimmune prostatitis (EAP) mice. Representative photographs of immunofluorescence staining for CCL20 and markers for (A) CD4 + T cells, (B) macrophages and (C, D) prostatic stromal cells of EAP mice. (E) Quantification of CCL20 immunofluorescence intensity in the experiments of (A–D). Representative data from three independent experiments are shown. Data were presented as mean ± SD and were analysed using one‐way anova analysis. * p < 0.05; ** p < 0.01; *** p < 0.001.

Journal: Journal of Cellular and Molecular Medicine

Article Title: Unraveling CCL20's role by regulating Th17 cell chemotaxis in experimental autoimmune prostatitis

doi: 10.1111/jcmm.18445

Figure Lengend Snippet: The potential source CCL20 in the prostate of experimental autoimmune prostatitis (EAP) mice. Representative photographs of immunofluorescence staining for CCL20 and markers for (A) CD4 + T cells, (B) macrophages and (C, D) prostatic stromal cells of EAP mice. (E) Quantification of CCL20 immunofluorescence intensity in the experiments of (A–D). Representative data from three independent experiments are shown. Data were presented as mean ± SD and were analysed using one‐way anova analysis. * p < 0.05; ** p < 0.01; *** p < 0.001.

Techniques: Immunofluorescence, Staining

IL‐17A promoted secretion of CCL20 of macrophages via the NF‐κB/MAPK/PI3K pathway. (A, B) Western blot analysis of CCL20 and the phosphorylation of the PI3K (mTOR and AKT) NF‐κB (P65) and MAPK (ERK1/2, P38) pathways in BMDM and RAW264.7 after treatment of LPS and/or rIL‐17. (C, D) Quantitative analysis of CCL20 in the supernatant of BMDM and RAW264.7 determined by ELISA. (E, F) Relative expression of CCL20 in BMDM and RAW264.7 measured by RT‐qPCR after treatment of LPS and/or rIL‐17A. (G, H) Western blot analysis of CCL20 after injection of rIL‐17A or anti‐IL‐17A neutralizing antibodies. (I, J) Quantitative analysis of CCL20 in the serum and prostate of mice determined by ELISA. Representative data from three independent experiments are shown. Data were presented as mean ± SD and were analysed using one‐way anova analysis. ‘ns’ p > 0.05; * p < 0.05; ** p < 0.01; *** p < 0.001.

Journal: Journal of Cellular and Molecular Medicine

Article Title: Unraveling CCL20's role by regulating Th17 cell chemotaxis in experimental autoimmune prostatitis

doi: 10.1111/jcmm.18445

Figure Lengend Snippet: IL‐17A promoted secretion of CCL20 of macrophages via the NF‐κB/MAPK/PI3K pathway. (A, B) Western blot analysis of CCL20 and the phosphorylation of the PI3K (mTOR and AKT) NF‐κB (P65) and MAPK (ERK1/2, P38) pathways in BMDM and RAW264.7 after treatment of LPS and/or rIL‐17. (C, D) Quantitative analysis of CCL20 in the supernatant of BMDM and RAW264.7 determined by ELISA. (E, F) Relative expression of CCL20 in BMDM and RAW264.7 measured by RT‐qPCR after treatment of LPS and/or rIL‐17A. (G, H) Western blot analysis of CCL20 after injection of rIL‐17A or anti‐IL‐17A neutralizing antibodies. (I, J) Quantitative analysis of CCL20 in the serum and prostate of mice determined by ELISA. Representative data from three independent experiments are shown. Data were presented as mean ± SD and were analysed using one‐way anova analysis. ‘ns’ p > 0.05; * p < 0.05; ** p < 0.01; *** p < 0.001.

Techniques: Western Blot, Phospho-proteomics, Enzyme-linked Immunosorbent Assay, Expressing, Quantitative RT-PCR, Injection

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