Review

mouse anti ccl22 antibody (R&D Systems)

Name: mouse anti ccl22 antibody
Brand: R&D Systems
Rating: 93 (4 reviews)

R&D Systems is a verified supplier

R&D Systems manufactures this product

About

News

Press Release

Team

Advisors

Partners

Contact

Bioz Stars

Bioz vStars

Buy from Supplier

Structured Review

R&D Systems mouse anti ccl22 antibody

( A ) GO analysis of macrophage response to LNR. ( B ) Heatmaps of macrophage-secreted chemokines in the iWAT from mice receiving sham or LNR at 6°C for 7 days ( n = 4 per group). Red and blue represent the fold increase and decrease in a gene, respectively (see color scale). ( C ) mRNA expression of macrophage-secreted chemokines in iWAT from mice described in (B) ( n = 8 per group). ( D ) <t>Ccl22</t> mRNA expression in iWAT from mice described in (B) at 23° or 6°C for 7 days ( n = 6 per group). ( E ) Ccl22 mRNA expression in iWAT from mice described in (B) exposed to 6°C for different hours ( n = 6). ( F ) Serum CCL22 levels from mice described in (B) exposed to 6°C for different days ( n = 6). ( G ) Serum CCL22 levels from mice described in (B) ( n = 6 per group). ( H ) Ccl22 mRNA expression in iWAT SVF cells or mature adipocytes (MAs). ( I ) Ccl22 mRNA expression in M0, M1, and M2 macrophages derived from 10-week-old C57BL/6 bone marrows ( n = 8 per group). ( J and K ) mRNA expression (J) and IF (K) of UCP1 in beige adipocytes ( n = 6 per group). Scale bars, 25 μm. ( L to N ) Immunofluorescence of UCP1 (L), mRNA expression of thermogenic genes (M), and immunoblots of UCP1 (N) in iWAT ( n = 3 to 6 per group). Scale bars, 50 μm. ( O to R ) Immunoblots and quantification of UCP1 [(O) and (P)], mRNA expression (Q) of thermogenic genes, and IF of UCP1 and H&E staining (R) in iWAT ( n = 3 to 6 per group). Scale bars, 50 μm. Data information: Results are presented as means ± SEM. [(C), (D), (G) to (J), (M), (P), and (Q)] * P ≤ 0.05, ** P < 0.01, and *** P < 0.001 by nonpaired Student’s t test. [(E) and (F)] * P ≤ 0.05 and ** P < 0.01 nonpaired Student’s t test compared with before cold stimulation.

Mouse Anti Ccl22 Antibody, supplied by R&D Systems, used in various techniques. Bioz Stars score: 93/100, based on 4 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/mouse anti ccl22 antibody/product/R&D Systems
Average 93 stars, based on 4 article reviews

mouse anti ccl22 antibody - by Bioz Stars, 2026-02

93/100 stars

Images

1) Product Images from "Macrophage-derived chemokine CCL22 establishes local LN-mediated adaptive thermogenesis and energy expenditure"

Article Title: Macrophage-derived chemokine CCL22 establishes local LN-mediated adaptive thermogenesis and energy expenditure

Journal: Science Advances

doi: 10.1126/sciadv.adn5229

Figure Legend Snippet: ( A ) GO analysis of macrophage response to LNR. ( B ) Heatmaps of macrophage-secreted chemokines in the iWAT from mice receiving sham or LNR at 6°C for 7 days ( n = 4 per group). Red and blue represent the fold increase and decrease in a gene, respectively (see color scale). ( C ) mRNA expression of macrophage-secreted chemokines in iWAT from mice described in (B) ( n = 8 per group). ( D ) Ccl22 mRNA expression in iWAT from mice described in (B) at 23° or 6°C for 7 days ( n = 6 per group). ( E ) Ccl22 mRNA expression in iWAT from mice described in (B) exposed to 6°C for different hours ( n = 6). ( F ) Serum CCL22 levels from mice described in (B) exposed to 6°C for different days ( n = 6). ( G ) Serum CCL22 levels from mice described in (B) ( n = 6 per group). ( H ) Ccl22 mRNA expression in iWAT SVF cells or mature adipocytes (MAs). ( I ) Ccl22 mRNA expression in M0, M1, and M2 macrophages derived from 10-week-old C57BL/6 bone marrows ( n = 8 per group). ( J and K ) mRNA expression (J) and IF (K) of UCP1 in beige adipocytes ( n = 6 per group). Scale bars, 25 μm. ( L to N ) Immunofluorescence of UCP1 (L), mRNA expression of thermogenic genes (M), and immunoblots of UCP1 (N) in iWAT ( n = 3 to 6 per group). Scale bars, 50 μm. ( O to R ) Immunoblots and quantification of UCP1 [(O) and (P)], mRNA expression (Q) of thermogenic genes, and IF of UCP1 and H&E staining (R) in iWAT ( n = 3 to 6 per group). Scale bars, 50 μm. Data information: Results are presented as means ± SEM. [(C), (D), (G) to (J), (M), (P), and (Q)] * P ≤ 0.05, ** P < 0.01, and *** P < 0.001 by nonpaired Student’s t test. [(E) and (F)] * P ≤ 0.05 and ** P < 0.01 nonpaired Student’s t test compared with before cold stimulation.

Techniques Used: Expressing, Derivative Assay, Immunofluorescence, Western Blot, Staining

( A ) Pearson’s correlation coefficient analysis of serum CCL22 concentration and fat mass ( n = 28 per group). ( B to F ) Body weight (B), energy consumption rate [(C) and (D)], and RER [(E) and (F)] ( n = 8 per group). Ten-week-old C57BL/6 male mice received saline or rCCL22 (20 μg/kg per day) at 6°C for 14 days with HFD. ( G to I ) Immunofluorescence (G), immunoblots (H) of UCP1, and mRNA expression (I) of thermogenic genes in iWAT ( n = 3 to 6 per group). Scale bar, 50 μm. ( J to L ) Immunofluorescence (J), immunoblots, and quantification [(K) and (L)] of UCP1 in iWAT ( n = 3 per group). SVF cells were extracted from HFD-fed iWAT, cultured with vehicle or rCCL22 (10 ng/ml) for 4 days, and then induced to beige adipocytes for 5 days. Scale bars, 25 μm. ( M ) Schematic diagram: The 6-month trial of obese adults participated in ADF: a 3-month weight loss period followed by a 3-month weight maintenance period. ( N and O ) Pearson’s correlation coefficient analysis of human serum CCL22 levels, body weight (N), and fat mass (O) ( n = 40). ( P ) Human serum CCL22 levels ( n = 20). ( Q ) Schematic diagram: Human SVFs from iWAT were cultured at 31°C for 5 days, treated with vehicle or CCL22 (10 ng/ml) for 4 days, and then induced to beige adipocytes. ( R to T ) Immunoblots and quantification [(R) and (S)] of UCP1 and mRNA expression (T) of thermogenic genes in human beige adipocytes ( n = 3 to 6 per group). Data information: Results are presented as means ± SEM. [(A), (N), and (O)] Two-tailed Pearson’s correlation coefficient analysis. [(F), (I), (L), (S), and (T)] * P ≤ 0.05 and ** P < 0.01 by nonpaired Student’s t test. (P) ** P < 0.01 by nonpaired Student’s t test compared with month 0 body weight. (B) * P ≤ 0.05 by two-way analysis of variance (ANOVA) followed by post hoc Bonferroni tests.

Figure Legend Snippet: ( A ) Pearson’s correlation coefficient analysis of serum CCL22 concentration and fat mass ( n = 28 per group). ( B to F ) Body weight (B), energy consumption rate [(C) and (D)], and RER [(E) and (F)] ( n = 8 per group). Ten-week-old C57BL/6 male mice received saline or rCCL22 (20 μg/kg per day) at 6°C for 14 days with HFD. ( G to I ) Immunofluorescence (G), immunoblots (H) of UCP1, and mRNA expression (I) of thermogenic genes in iWAT ( n = 3 to 6 per group). Scale bar, 50 μm. ( J to L ) Immunofluorescence (J), immunoblots, and quantification [(K) and (L)] of UCP1 in iWAT ( n = 3 per group). SVF cells were extracted from HFD-fed iWAT, cultured with vehicle or rCCL22 (10 ng/ml) for 4 days, and then induced to beige adipocytes for 5 days. Scale bars, 25 μm. ( M ) Schematic diagram: The 6-month trial of obese adults participated in ADF: a 3-month weight loss period followed by a 3-month weight maintenance period. ( N and O ) Pearson’s correlation coefficient analysis of human serum CCL22 levels, body weight (N), and fat mass (O) ( n = 40). ( P ) Human serum CCL22 levels ( n = 20). ( Q ) Schematic diagram: Human SVFs from iWAT were cultured at 31°C for 5 days, treated with vehicle or CCL22 (10 ng/ml) for 4 days, and then induced to beige adipocytes. ( R to T ) Immunoblots and quantification [(R) and (S)] of UCP1 and mRNA expression (T) of thermogenic genes in human beige adipocytes ( n = 3 to 6 per group). Data information: Results are presented as means ± SEM. [(A), (N), and (O)] Two-tailed Pearson’s correlation coefficient analysis. [(F), (I), (L), (S), and (T)] * P ≤ 0.05 and ** P < 0.01 by nonpaired Student’s t test. (P) ** P < 0.01 by nonpaired Student’s t test compared with month 0 body weight. (B) * P ≤ 0.05 by two-way analysis of variance (ANOVA) followed by post hoc Bonferroni tests.

Techniques Used: Concentration Assay, Saline, Immunofluorescence, Western Blot, Expressing, Cell Culture, Two Tailed Test

Figure Legend Snippet: Primer sequences for qPCR gene expression analysis.

Techniques Used: Expressing

Image Search Results

Journal: Science Advances

Article Title: Macrophage-derived chemokine CCL22 establishes local LN-mediated adaptive thermogenesis and energy expenditure

doi: 10.1126/sciadv.adn5229

Figure Lengend Snippet: ( A ) GO analysis of macrophage response to LNR. ( B ) Heatmaps of macrophage-secreted chemokines in the iWAT from mice receiving sham or LNR at 6°C for 7 days ( n = 4 per group). Red and blue represent the fold increase and decrease in a gene, respectively (see color scale). ( C ) mRNA expression of macrophage-secreted chemokines in iWAT from mice described in (B) ( n = 8 per group). ( D ) Ccl22 mRNA expression in iWAT from mice described in (B) at 23° or 6°C for 7 days ( n = 6 per group). ( E ) Ccl22 mRNA expression in iWAT from mice described in (B) exposed to 6°C for different hours ( n = 6). ( F ) Serum CCL22 levels from mice described in (B) exposed to 6°C for different days ( n = 6). ( G ) Serum CCL22 levels from mice described in (B) ( n = 6 per group). ( H ) Ccl22 mRNA expression in iWAT SVF cells or mature adipocytes (MAs). ( I ) Ccl22 mRNA expression in M0, M1, and M2 macrophages derived from 10-week-old C57BL/6 bone marrows ( n = 8 per group). ( J and K ) mRNA expression (J) and IF (K) of UCP1 in beige adipocytes ( n = 6 per group). Scale bars, 25 μm. ( L to N ) Immunofluorescence of UCP1 (L), mRNA expression of thermogenic genes (M), and immunoblots of UCP1 (N) in iWAT ( n = 3 to 6 per group). Scale bars, 50 μm. ( O to R ) Immunoblots and quantification of UCP1 [(O) and (P)], mRNA expression (Q) of thermogenic genes, and IF of UCP1 and H&E staining (R) in iWAT ( n = 3 to 6 per group). Scale bars, 50 μm. Data information: Results are presented as means ± SEM. [(C), (D), (G) to (J), (M), (P), and (Q)] * P ≤ 0.05, ** P < 0.01, and *** P < 0.001 by nonpaired Student’s t test. [(E) and (F)] * P ≤ 0.05 and ** P < 0.01 nonpaired Student’s t test compared with before cold stimulation.

Article Snippet: Total protein lysates (20 μg) were immunoblotted with rabbit anti–p-FAK (Y397) (1:1000; ABclonal, #AP0302), rabbit anti-FAK (1:1000; ABclonal, A11195), rabbit anti-p65 antibody (1:1000; Abcam, ab32536), rabbit anti-CCR4 antibody (1:1000; Novus Biological, NB56336SS), rabbit anti-UCP1 antibody (1:500; Abcam, ab23841), rabbit anti-tubulin antibody [1:2000; Cell Signaling Technology (CST), 2146S], mouse anti-CCL22 antibody (1:1000; R&D Systems, MAB439-SP), mouse anti-CD206 antibody (Bio-Rad, MAC2235GA), rat anti-F4/80 (1:500; Abcam, ab6640), rat anti-siglecF (1:500; Novus Biological, NBP1-91149), rabbit anti–IL-13 antibody (1:500; ABclonal, A2089), rabbit anti-p-STAT6 antibody (1:500; ABclonal, AP0456), rabbit anti-STAT6 antibody (1:500; ABclonal, A0755), rabbit anti-Histone3 antibody (1:1000; CST, 4499P), followed by goat anti-rat horseradish peroxidase (HRP)–conjugated secondary antibody (1:5000; ABconal, AS028), anti-rabbit HRP-conjugated secondary antibody (1:5000; CST, 7074S), goat anti-mouse HRP-conjugated secondary antibody (1:5000; CST, 96714S).

Techniques: Expressing, Derivative Assay, Immunofluorescence, Western Blot, Staining

Journal: Science Advances

Article Title: Macrophage-derived chemokine CCL22 establishes local LN-mediated adaptive thermogenesis and energy expenditure

doi: 10.1126/sciadv.adn5229

Figure Lengend Snippet: ( A ) Pearson’s correlation coefficient analysis of serum CCL22 concentration and fat mass ( n = 28 per group). ( B to F ) Body weight (B), energy consumption rate [(C) and (D)], and RER [(E) and (F)] ( n = 8 per group). Ten-week-old C57BL/6 male mice received saline or rCCL22 (20 μg/kg per day) at 6°C for 14 days with HFD. ( G to I ) Immunofluorescence (G), immunoblots (H) of UCP1, and mRNA expression (I) of thermogenic genes in iWAT ( n = 3 to 6 per group). Scale bar, 50 μm. ( J to L ) Immunofluorescence (J), immunoblots, and quantification [(K) and (L)] of UCP1 in iWAT ( n = 3 per group). SVF cells were extracted from HFD-fed iWAT, cultured with vehicle or rCCL22 (10 ng/ml) for 4 days, and then induced to beige adipocytes for 5 days. Scale bars, 25 μm. ( M ) Schematic diagram: The 6-month trial of obese adults participated in ADF: a 3-month weight loss period followed by a 3-month weight maintenance period. ( N and O ) Pearson’s correlation coefficient analysis of human serum CCL22 levels, body weight (N), and fat mass (O) ( n = 40). ( P ) Human serum CCL22 levels ( n = 20). ( Q ) Schematic diagram: Human SVFs from iWAT were cultured at 31°C for 5 days, treated with vehicle or CCL22 (10 ng/ml) for 4 days, and then induced to beige adipocytes. ( R to T ) Immunoblots and quantification [(R) and (S)] of UCP1 and mRNA expression (T) of thermogenic genes in human beige adipocytes ( n = 3 to 6 per group). Data information: Results are presented as means ± SEM. [(A), (N), and (O)] Two-tailed Pearson’s correlation coefficient analysis. [(F), (I), (L), (S), and (T)] * P ≤ 0.05 and ** P < 0.01 by nonpaired Student’s t test. (P) ** P < 0.01 by nonpaired Student’s t test compared with month 0 body weight. (B) * P ≤ 0.05 by two-way analysis of variance (ANOVA) followed by post hoc Bonferroni tests.

Techniques: Concentration Assay, Saline, Immunofluorescence, Western Blot, Expressing, Cell Culture, Two Tailed Test

Journal: Science Advances

Article Title: Macrophage-derived chemokine CCL22 establishes local LN-mediated adaptive thermogenesis and energy expenditure

doi: 10.1126/sciadv.adn5229

Figure Lengend Snippet: Primer sequences for qPCR gene expression analysis.

Techniques: Expressing

Identification of CCL22 as a target for treatment of contact allergy and development of aptamers targeting murine CCL22 (A) Time line of the CHS mouse model. (B) The ear swelling response in CCL22 −/− mice in the CHS model is significantly reduced compared to WT mice ( n = 7, mean ± SEM). Data were tested for statistical significance by 2-way ANOVA with Bonferroni post hoc test (∗ p = 0.01–0.05; ∗∗ p = 0.001–0.01; ∗∗∗ p < 0.001; ∗∗∗∗ p < 0.0001). (C) Flow cytometry-based interaction analysis of enriched DNA libraries from the SL and selection cycles 5, 8, and 10 to murine CCL22. (D) Frequency of unique sequences in selection cycles 3, 6, 8, and 10. The frequency was calculated by dividing the overall number of sequences by the number of unique sequences. (E) Number of sequence reads in the NGS analysis per selection cycle. (F) Fraction of sequences in the DNA population from selection cycles 3, 6, 8, and 10 sharing the indicated copy numbers. (G and H) Nucleotide distribution in the random region of the SL and library from selection cycle 10. The nucleotides are evenly distributed in the SL, and preferences for particular nucleotides at certain positions evolve during the selection. (I) Frequency of the most enriched sequences in selection cycles 3, 6, 8, and 10. Missing data points indicate that the sequence could not be detected in the NGS data of the respective round. (J) DNA sequences identified by NGS were analyzed for binding to murine CCL22 by ELONA ( n = 2, mean ± SD).

Journal: Molecular Therapy. Nucleic Acids

Article Title: Topical application of a CCL22-binding aptamer suppresses contact allergy

doi: 10.1016/j.omtn.2024.102254

Figure Lengend Snippet: Identification of CCL22 as a target for treatment of contact allergy and development of aptamers targeting murine CCL22 (A) Time line of the CHS mouse model. (B) The ear swelling response in CCL22 −/− mice in the CHS model is significantly reduced compared to WT mice ( n = 7, mean ± SEM). Data were tested for statistical significance by 2-way ANOVA with Bonferroni post hoc test (∗ p = 0.01–0.05; ∗∗ p = 0.001–0.01; ∗∗∗ p < 0.001; ∗∗∗∗ p < 0.0001). (C) Flow cytometry-based interaction analysis of enriched DNA libraries from the SL and selection cycles 5, 8, and 10 to murine CCL22. (D) Frequency of unique sequences in selection cycles 3, 6, 8, and 10. The frequency was calculated by dividing the overall number of sequences by the number of unique sequences. (E) Number of sequence reads in the NGS analysis per selection cycle. (F) Fraction of sequences in the DNA population from selection cycles 3, 6, 8, and 10 sharing the indicated copy numbers. (G and H) Nucleotide distribution in the random region of the SL and library from selection cycle 10. The nucleotides are evenly distributed in the SL, and preferences for particular nucleotides at certain positions evolve during the selection. (I) Frequency of the most enriched sequences in selection cycles 3, 6, 8, and 10. Missing data points indicate that the sequence could not be detected in the NGS data of the respective round. (J) DNA sequences identified by NGS were analyzed for binding to murine CCL22 by ELONA ( n = 2, mean ± SD).

Article Snippet: Coupling of CCL22 on carboxyl beads was validated by staining with an anti-CCL22 antibody (mouse α-murine CCL22 [R&D Systems]) and fluorescently labeled secondary antibody (goat α-mouse Alexa Fluor 647 (Jackson ImmunoResearch) by flow cytometry.

Techniques: Flow Cytometry, Selection, Sequencing, Binding Assay

Aptamer-dependent inhibition of migration toward mCCL22 in vitro and motifs enriched during CCL22 SELEX (A–H) Migration of BW5147.3 cells toward CCL22 (12.8 nM) was measured in a transwell migration assay in the presence of aptamers. Full-length aptamers AJ1 (A), AJ21 (B), AJ25 (C), AJ78 (D), AJ81 (E), AJ82 (F), AJ102 (G), and AJ104 (H) were tested in a 1:10 M ratio (1.28 nM), an equimolar ratio (12.8 nM), and a 10:1 M ratio (128 nM) along with their scrambled control sequences. As control, migration without the addition of CCL22 or aptamers, as well as the migration toward CCL22 only were measured. Statistical significance was calculated against migration toward CCL22 and tested by using ordinary 1-way ANOVA with post hoc Bonferroni test with n = 3–16 (mean ± SEM, ∗ p = 0.01–0.05; ∗∗ p = 0.001–0.01; ∗∗∗ p < 0.001; ∗∗∗∗ p < 0.0001). (I) Frequency of 3 motifs common among the most enriched sequences. Motif 1 is found in AJ81 and AJ82. Motif 2 is found in AJ1, AJ25, and AJ104. Motif 3 is found in AJ21 and AJ102. (J) Sequences of the motifs identified by MEME Suite.

Journal: Molecular Therapy. Nucleic Acids

Article Title: Topical application of a CCL22-binding aptamer suppresses contact allergy

doi: 10.1016/j.omtn.2024.102254

Figure Lengend Snippet: Aptamer-dependent inhibition of migration toward mCCL22 in vitro and motifs enriched during CCL22 SELEX (A–H) Migration of BW5147.3 cells toward CCL22 (12.8 nM) was measured in a transwell migration assay in the presence of aptamers. Full-length aptamers AJ1 (A), AJ21 (B), AJ25 (C), AJ78 (D), AJ81 (E), AJ82 (F), AJ102 (G), and AJ104 (H) were tested in a 1:10 M ratio (1.28 nM), an equimolar ratio (12.8 nM), and a 10:1 M ratio (128 nM) along with their scrambled control sequences. As control, migration without the addition of CCL22 or aptamers, as well as the migration toward CCL22 only were measured. Statistical significance was calculated against migration toward CCL22 and tested by using ordinary 1-way ANOVA with post hoc Bonferroni test with n = 3–16 (mean ± SEM, ∗ p = 0.01–0.05; ∗∗ p = 0.001–0.01; ∗∗∗ p < 0.001; ∗∗∗∗ p < 0.0001). (I) Frequency of 3 motifs common among the most enriched sequences. Motif 1 is found in AJ81 and AJ82. Motif 2 is found in AJ1, AJ25, and AJ104. Motif 3 is found in AJ21 and AJ102. (J) Sequences of the motifs identified by MEME Suite.

Techniques: Inhibition, Migration, In Vitro, Transwell Migration Assay, Control

Binding affinity and specificity of aptamer AJ82 and AJ102 (A and B) Concentration-dependent binding of aptamer AJ82 (A) and AJ102 (B) measured by SPR using murine CCL22 as analyte and biotinylated aptamers as immobilized ligands ( n = 2, mean ± SD). (C) Table of kinetic properties of the aptamers AJ82, AJ82.51, AJ102, and AJ102.29 as measured by flow cytometry or SPR. nd, not determined. (D) Interaction analysis of aptamer AJ82 and AJ102 with murine CCL22, human CCL22, murine CCL17, human CCL17, and human CCL3 measured by an ELONA ( n = 2–3, mean ± SD).

Journal: Molecular Therapy. Nucleic Acids

Article Title: Topical application of a CCL22-binding aptamer suppresses contact allergy

doi: 10.1016/j.omtn.2024.102254

Figure Lengend Snippet: Binding affinity and specificity of aptamer AJ82 and AJ102 (A and B) Concentration-dependent binding of aptamer AJ82 (A) and AJ102 (B) measured by SPR using murine CCL22 as analyte and biotinylated aptamers as immobilized ligands ( n = 2, mean ± SD). (C) Table of kinetic properties of the aptamers AJ82, AJ82.51, AJ102, and AJ102.29 as measured by flow cytometry or SPR. nd, not determined. (D) Interaction analysis of aptamer AJ82 and AJ102 with murine CCL22, human CCL22, murine CCL17, human CCL17, and human CCL3 measured by an ELONA ( n = 2–3, mean ± SD).

Techniques: Binding Assay, Concentration Assay, Flow Cytometry

Truncation of aptamers and specificity of AJ82.51 and AJ102.29 (A) Flow cytometry-based interaction assay of truncated variants of aptamer AJ82 with CCL22. AJ82 was truncated from 80 to 51 nt, including an initial point mutation at position 49 (dA to dC) for stabilization of the stem structure. (B and C) Structure predictions of aptamer AJ82 (B) and AJ102 (C) as predicted by Mfold web server. Shown is the prediction for the full-length sequence. Colored nucleotides indicate the motif 1 in AJ82 and motif 2 in AJ102. Gray nucleotides were truncated. (D) Flow cytometry-based interaction assay of truncated variants of aptamer AJ102 with CCL22. AJ102.29 was truncated from 80 to 29 nucleotides. AJ102.24 was truncated from the 5′ end, while AJ102.25 was truncated from the 3′ end ( n = 2, mean ± SD). (E) Flow cytometry-based interaction analysis with AJ102 and point mutants within the motif region ( n = 2, mean ± SD). Mainly dG positions are involved in target binding. (F and G) Interaction analysis of truncated 500-nM aptamers AJ82.51 (F) or AJ102.29 (G) with related chemokines human CCL22, murine and human CCL17, human CCL3, human CXCL1, human CXCL9, human CXCL10, human CXCL11 and unrelated proteins human serum albumin (HSA) and mitogen-activated protein kinase 1 (Erk2) measured by ELONA ( n = 2, mean ± SD).

Journal: Molecular Therapy. Nucleic Acids

Article Title: Topical application of a CCL22-binding aptamer suppresses contact allergy

doi: 10.1016/j.omtn.2024.102254

Figure Lengend Snippet: Truncation of aptamers and specificity of AJ82.51 and AJ102.29 (A) Flow cytometry-based interaction assay of truncated variants of aptamer AJ82 with CCL22. AJ82 was truncated from 80 to 51 nt, including an initial point mutation at position 49 (dA to dC) for stabilization of the stem structure. (B and C) Structure predictions of aptamer AJ82 (B) and AJ102 (C) as predicted by Mfold web server. Shown is the prediction for the full-length sequence. Colored nucleotides indicate the motif 1 in AJ82 and motif 2 in AJ102. Gray nucleotides were truncated. (D) Flow cytometry-based interaction assay of truncated variants of aptamer AJ102 with CCL22. AJ102.29 was truncated from 80 to 29 nucleotides. AJ102.24 was truncated from the 5′ end, while AJ102.25 was truncated from the 3′ end ( n = 2, mean ± SD). (E) Flow cytometry-based interaction analysis with AJ102 and point mutants within the motif region ( n = 2, mean ± SD). Mainly dG positions are involved in target binding. (F and G) Interaction analysis of truncated 500-nM aptamers AJ82.51 (F) or AJ102.29 (G) with related chemokines human CCL22, murine and human CCL17, human CCL3, human CXCL1, human CXCL9, human CXCL10, human CXCL11 and unrelated proteins human serum albumin (HSA) and mitogen-activated protein kinase 1 (Erk2) measured by ELONA ( n = 2, mean ± SD).

Techniques: Flow Cytometry, Mutagenesis, Sequencing, Binding Assay

Inhibition of CCL22 mediated cell migration in vitro by truncated and modified aptamers AJ82.51 and AJ102.29 (A) Schematic representation of the transwell migration assay. BW5147.3 cells were placed in the upper layer of the insert with a permeable membrane, and CCL22 was added at different concentrations to the lower compartment. Following an incubation period, the cells that migrated through the membrane were quantified by flow cytometry. (B and C) Migration of BW5147.3 cells toward CCL22 (12.8 nM) was measured in a transwell migration assay in the presence of aptamers. Truncated aptamers AJ82.51 (B) and AJ102.29 (C) and truncated and modified aptamers AJ82.51m (B) and AJ102.29m (C) were tested in a 1:10 M ratio (1.28 nM), an equimolar ratio (12.8 nM), and a 10:1 M ratio (128 nM). As control, migration toward the control sequences AJ82.51 ctrl, AJ102.29 ctrl and AJ82.51m ctrl, AJ102.29m ctrl (12.8 nM), without the addition of CCL22 or aptamers, as well as the migration toward CCL22 only were measured. Statistical significance was calculated against migration toward CCL22 and tested by using ordinary 1-way ANOVA with post hoc Bonferroni test, with n = 7–15 (mean ± SEM; ∗∗∗∗ p < 0.0001). ns, not significant.

Journal: Molecular Therapy. Nucleic Acids

Article Title: Topical application of a CCL22-binding aptamer suppresses contact allergy

doi: 10.1016/j.omtn.2024.102254

Figure Lengend Snippet: Inhibition of CCL22 mediated cell migration in vitro by truncated and modified aptamers AJ82.51 and AJ102.29 (A) Schematic representation of the transwell migration assay. BW5147.3 cells were placed in the upper layer of the insert with a permeable membrane, and CCL22 was added at different concentrations to the lower compartment. Following an incubation period, the cells that migrated through the membrane were quantified by flow cytometry. (B and C) Migration of BW5147.3 cells toward CCL22 (12.8 nM) was measured in a transwell migration assay in the presence of aptamers. Truncated aptamers AJ82.51 (B) and AJ102.29 (C) and truncated and modified aptamers AJ82.51m (B) and AJ102.29m (C) were tested in a 1:10 M ratio (1.28 nM), an equimolar ratio (12.8 nM), and a 10:1 M ratio (128 nM). As control, migration toward the control sequences AJ82.51 ctrl, AJ102.29 ctrl and AJ82.51m ctrl, AJ102.29m ctrl (12.8 nM), without the addition of CCL22 or aptamers, as well as the migration toward CCL22 only were measured. Statistical significance was calculated against migration toward CCL22 and tested by using ordinary 1-way ANOVA with post hoc Bonferroni test, with n = 7–15 (mean ± SEM; ∗∗∗∗ p < 0.0001). ns, not significant.

Techniques: Inhibition, Migration, In Vitro, Modification, Transwell Migration Assay, Membrane, Incubation, Flow Cytometry, Control

Ex vivo and in vivo application of AJ102.29 results in effective reduction of contact hypersensitivity symptoms and penetration of the skin (A) Time line of the contact hypersensitivity model application time points of AJ102.29m. (B) Ear swelling of WT mice that received PBS, 10 nmol AJ102.29m, or 10 nmol AJ102.29mctrl intraperitoneally and of CCL22 −/− mice 24 h (day 1), 48 h (day 2), and 72 h (day 3) after application of DNFB (solid lines) or vehicle (dashed lines). Data were tested for statistical significance by 2-way ANOVA with Bonferroni post hoc test ( n = 6 WT PBS, WT AJ102.29 ctrl, WT AJ102.29 ctrl, n = 3 CCL22 −/− , mean ± SEM; ∗ p = 0.01–0.05; ∗∗ p = 0.001–0.01; ∗∗∗ p < 0.001; ∗∗∗∗ p < 0.0001). (C) Schematic representation of the Franz-diffusion cell assay. Fluorescently labeled aptamer in DAC cream was placed in the donor compartment. The skin of a mouse ear was placed horizontally between the donor and receptor compartment filled with RPMI medium. After 24 h the skin sample was stained with DAPI and analyzed by fluorescent micrsocopy to investigate skin penetration of the aptamer. (D) DAPI-stained sections of mouse ears treated with DAC cream with or without Atto647 labeled AJ102.29 (10 pmol mg −1 ) in an ex vivo Franz-diffusion cell assay. (E) Ear swelling of WT mice that received PBS, 10 nmol AJ102.29m, or AJ102.29mctrl mixed in a DAC cream and topically applied on the ear at the time of and 12 h after challenge, and of CCL22 −/− mice 24 h (day 1), 48 h (day 2), and 72 h (day 3) after application of DNFB (solid lines) or vehicle (dashed lines) ( n = 4–5, mean ± SEM). Data were tested for statistical significance by 2-way ANOVA with Bonferroni post hoc test ( n = 5 per group, mean ± SEM; ∗ p = 0.01–0.05; ∗∗ p = 0.001–0.01; ∗∗∗ p < 0.001; ∗∗∗∗ p < 0.0001).

Journal: Molecular Therapy. Nucleic Acids

Article Title: Topical application of a CCL22-binding aptamer suppresses contact allergy

doi: 10.1016/j.omtn.2024.102254

Figure Lengend Snippet: Ex vivo and in vivo application of AJ102.29 results in effective reduction of contact hypersensitivity symptoms and penetration of the skin (A) Time line of the contact hypersensitivity model application time points of AJ102.29m. (B) Ear swelling of WT mice that received PBS, 10 nmol AJ102.29m, or 10 nmol AJ102.29mctrl intraperitoneally and of CCL22 −/− mice 24 h (day 1), 48 h (day 2), and 72 h (day 3) after application of DNFB (solid lines) or vehicle (dashed lines). Data were tested for statistical significance by 2-way ANOVA with Bonferroni post hoc test ( n = 6 WT PBS, WT AJ102.29 ctrl, WT AJ102.29 ctrl, n = 3 CCL22 −/− , mean ± SEM; ∗ p = 0.01–0.05; ∗∗ p = 0.001–0.01; ∗∗∗ p < 0.001; ∗∗∗∗ p < 0.0001). (C) Schematic representation of the Franz-diffusion cell assay. Fluorescently labeled aptamer in DAC cream was placed in the donor compartment. The skin of a mouse ear was placed horizontally between the donor and receptor compartment filled with RPMI medium. After 24 h the skin sample was stained with DAPI and analyzed by fluorescent micrsocopy to investigate skin penetration of the aptamer. (D) DAPI-stained sections of mouse ears treated with DAC cream with or without Atto647 labeled AJ102.29 (10 pmol mg −1 ) in an ex vivo Franz-diffusion cell assay. (E) Ear swelling of WT mice that received PBS, 10 nmol AJ102.29m, or AJ102.29mctrl mixed in a DAC cream and topically applied on the ear at the time of and 12 h after challenge, and of CCL22 −/− mice 24 h (day 1), 48 h (day 2), and 72 h (day 3) after application of DNFB (solid lines) or vehicle (dashed lines) ( n = 4–5, mean ± SEM). Data were tested for statistical significance by 2-way ANOVA with Bonferroni post hoc test ( n = 5 per group, mean ± SEM; ∗ p = 0.01–0.05; ∗∗ p = 0.001–0.01; ∗∗∗ p < 0.001; ∗∗∗∗ p < 0.0001).

Techniques: Ex Vivo, In Vivo, Diffusion-based Assay, Labeling, Cream, Staining

A . Differentially expressed genes in unstimulated or LPS or IL-4 stimulated LysM ΔZeb1 compared to LysM Ctrl BMDMs as measured by a customized RT2 array and depicted in log 2 fold change of expression. nd marks non-detectable mRNA levels. All transcripts were normalized to Gapdh (n=3). B . Relative mRNA expression of Ccl2 and Ccl22 in LysM Ctrl and LysM ΔZeb1 BMDMs (n=3; means ±SD; 2-way ANOVA). C . Comparison of transcript and secretome alterations of Ccl2 and Ccl22 in LysM ΔZeb1 compared to LysM Ctrl BMDMs (n≥5; means ±SD).

Journal: bioRxiv

Article Title: Macrophages foster adaptive anti-tumor immunity by ZEB1-dependent cytotoxic T cell chemoattraction

doi: 10.1101/2024.02.26.582102

Figure Lengend Snippet: A . Differentially expressed genes in unstimulated or LPS or IL-4 stimulated LysM ΔZeb1 compared to LysM Ctrl BMDMs as measured by a customized RT2 array and depicted in log 2 fold change of expression. nd marks non-detectable mRNA levels. All transcripts were normalized to Gapdh (n=3). B . Relative mRNA expression of Ccl2 and Ccl22 in LysM Ctrl and LysM ΔZeb1 BMDMs (n=3; means ±SD; 2-way ANOVA). C . Comparison of transcript and secretome alterations of Ccl2 and Ccl22 in LysM ΔZeb1 compared to LysM Ctrl BMDMs (n≥5; means ±SD).

Article Snippet: Final concentrations of cytokines were 1.93 ng/ ml CCL2 (R&D Systems, 479-JE-050) and 0.18 ng/ ml CCL22 (R&D Systems, 439-MD-025) and of antibodies 5 μg/ml IgG (Diagenode, C15410206), anti-CCL2 (Novus Biologicals, NBP1-07035SS) or anti-CCL22 (abcam, ab124768), respectively.

Techniques: Expressing, Comparison

A-B . Venn diagrams of differentially expressed genes (DEGs) of LysM Ctrl (blue) and LysM ΔZeb1 BMDMs (red) after stimulation with LPS (A) or IL-4 (B) compared to unstimulated in total (left) and divided in up-/downregulated DEGs (right). C . GO term enrichment analysis for DEGs (FDR<0.05) uniquely up- or downregulated by LysM ΔZeb1 BMDMs after LPS stimulation. D . Log 2 fold change of expression of selected trafficking genes after LPS stimulation. X marks no significant deregulation. E . Representative images and quantification of OPP incorporation of LysM Ctrl and LysM ΔZeb1 BMDMs with 0h, 4h and 16h LPS pre-stimulation (n=3; means ±SD; 2-way ANOVA). F-G . Representative arrays of intracellular cytokines of LysM Ctrl and LysM ΔZeb1 BMDMs with LPS stimulation or additional Brefeldin A and Monensin treatment (F) and quantification of intracellular CCL2 and CCL22 after LPS, Brefeldin A and Monensin treatment (G; n≥2).

Journal: bioRxiv

Article Title: Macrophages foster adaptive anti-tumor immunity by ZEB1-dependent cytotoxic T cell chemoattraction

doi: 10.1101/2024.02.26.582102

Figure Lengend Snippet: A-B . Venn diagrams of differentially expressed genes (DEGs) of LysM Ctrl (blue) and LysM ΔZeb1 BMDMs (red) after stimulation with LPS (A) or IL-4 (B) compared to unstimulated in total (left) and divided in up-/downregulated DEGs (right). C . GO term enrichment analysis for DEGs (FDR<0.05) uniquely up- or downregulated by LysM ΔZeb1 BMDMs after LPS stimulation. D . Log 2 fold change of expression of selected trafficking genes after LPS stimulation. X marks no significant deregulation. E . Representative images and quantification of OPP incorporation of LysM Ctrl and LysM ΔZeb1 BMDMs with 0h, 4h and 16h LPS pre-stimulation (n=3; means ±SD; 2-way ANOVA). F-G . Representative arrays of intracellular cytokines of LysM Ctrl and LysM ΔZeb1 BMDMs with LPS stimulation or additional Brefeldin A and Monensin treatment (F) and quantification of intracellular CCL2 and CCL22 after LPS, Brefeldin A and Monensin treatment (G; n≥2).

Techniques: Expressing

A . Confluence of KPC cells alone or co-cultured with LysM Ctrl or LysM ΔZeb1 BMDMs (n=3). B . Representative images at t=28h and quantification over time of KPC cell invasion into a scratch wound without or with co-culture of LysM Ctrl or LysM ΔZeb1 BMDMs (n=3). C . Confluence of KPC cells alone or with LysM Ctrl or LysM ΔZeb1 BMDM conditioned medium (CM) (n=2 KPC CM, n=3 LysM Ctrl and LysM ΔZeb1 CM). D . Transwell migration assay of CD8+ T cells alone or towards LysM Ctrl or LysM ΔZeb1 BMDMs in absence or presence of recombinant CCL2 and CCL22 (left panel, n>3) or absence or presence of anti-CCL2 and anti-CCL22 antibodies (right panel, n=3). Means ±SD; *:p<0.05; **:p<0.01; ns: not significant; 2-way ANOVA.

Journal: bioRxiv

Article Title: Macrophages foster adaptive anti-tumor immunity by ZEB1-dependent cytotoxic T cell chemoattraction

doi: 10.1101/2024.02.26.582102

Figure Lengend Snippet: A . Confluence of KPC cells alone or co-cultured with LysM Ctrl or LysM ΔZeb1 BMDMs (n=3). B . Representative images at t=28h and quantification over time of KPC cell invasion into a scratch wound without or with co-culture of LysM Ctrl or LysM ΔZeb1 BMDMs (n=3). C . Confluence of KPC cells alone or with LysM Ctrl or LysM ΔZeb1 BMDM conditioned medium (CM) (n=2 KPC CM, n=3 LysM Ctrl and LysM ΔZeb1 CM). D . Transwell migration assay of CD8+ T cells alone or towards LysM Ctrl or LysM ΔZeb1 BMDMs in absence or presence of recombinant CCL2 and CCL22 (left panel, n>3) or absence or presence of anti-CCL2 and anti-CCL22 antibodies (right panel, n=3). Means ±SD; *:p<0.05; **:p<0.01; ns: not significant; 2-way ANOVA.

Techniques: Cell Culture, Co-Culture Assay, Transwell Migration Assay, Recombinant

FIGURE 1 Circulating CCL17 and CCL22 chemokine levels in morbidly obese patients and age-matched controls. (A) CCL17 and (B) CCL22 levels were measured in plasma samples from obese patients (n = 60) and controls (n = 20). Scatter dot plots showing median with interquartile range. Comparison between groups were made by Mann Whitney test. Spearman test shows a positive correlation between CCL17 and CCL22 with HOMA- IR Index (C, D) and BMI (E, F) (n = 20 control subjects and n = 60 morbidly obese patients).

Journal: Frontiers in endocrinology

Article Title: CCL17 and CCL22 chemokines are upregulated in human obesity and play a role in vascular dysfunction.

doi: 10.3389/fendo.2023.1154158

Figure Lengend Snippet: FIGURE 1 Circulating CCL17 and CCL22 chemokine levels in morbidly obese patients and age-matched controls. (A) CCL17 and (B) CCL22 levels were measured in plasma samples from obese patients (n = 60) and controls (n = 20). Scatter dot plots showing median with interquartile range. Comparison between groups were made by Mann Whitney test. Spearman test shows a positive correlation between CCL17 and CCL22 with HOMA- IR Index (C, D) and BMI (E, F) (n = 20 control subjects and n = 60 morbidly obese patients).

Article Snippet: Antigen was unmasked with proteinase K (cat#S3020, Dako, Santa Clara, CA) and blocked with 15% horse serum for 1 h. Samples were incubated with the following primary antibodies overnight at 4°C: mouse anti-human CCL17 (1:50, cat#DY364-05, R&D Systems), mouse anti-human CCL22 (1:50, cat#DY336, R&D Systems), goat anti-human CCR4 (1:100, ab1669; Abcam, Cambridge, UK), rabbit anti-human CD3 (1:100, cat#C7930, Sigma-Aldrich, St. Louis, MO), rabbit polyclonal anti-human CD31 (1:50, cat#ab32457, Abcam) and rat anti-human Mac-3 (1:100, cat#sc19991, Santa Cruz Biotechnology, Dallas, TX).

Techniques: Clinical Proteomics, Comparison, MANN-WHITNEY, Control

FIGURE 2 Expression of CCL17 and CCL22 is increased in VCAT from morbidly obese patients. Relative quantiﬁcation of mRNA levels for (A) CCL17 and (B) CCL22. Comparisons between groups were made by Wilcoxon matched-pair signed-rank test. Values are expressed as mean ± SEM (n = 33). (C) CCL17 and (D) CCL22 chemokine release into conditioned media was determined after 48 h of SCAT and VCAT explant culture. Chemokine secretion is expressed as pg/ml in the supernatant. Values are expressed as mean ± SEM (n = 22). Comparison between groups were made by Mann Whitney test. (E) Immunoﬂuorescence representative images showing colocalization of CCL17 with CD3 (lymphocytes), CD31 (endothelial cells) and Mac-3 (macrophages); or CCL22 with CD3, CD31, Mac-3 in VCAT. Immunoreactivity was visualized using Alexa Fluor 594 (CCL17 and CCL22, red) and Alexa Fluor 488 (CD31, CD3, Mac-3, green) secondary antibodies. Nuclei were stained with Hoechst (blue). Scale bar, 20 mm. Nuclei were stained with Hoechst (blue).

Journal: Frontiers in endocrinology

Article Title: CCL17 and CCL22 chemokines are upregulated in human obesity and play a role in vascular dysfunction.

doi: 10.3389/fendo.2023.1154158

Figure Lengend Snippet: FIGURE 2 Expression of CCL17 and CCL22 is increased in VCAT from morbidly obese patients. Relative quantiﬁcation of mRNA levels for (A) CCL17 and (B) CCL22. Comparisons between groups were made by Wilcoxon matched-pair signed-rank test. Values are expressed as mean ± SEM (n = 33). (C) CCL17 and (D) CCL22 chemokine release into conditioned media was determined after 48 h of SCAT and VCAT explant culture. Chemokine secretion is expressed as pg/ml in the supernatant. Values are expressed as mean ± SEM (n = 22). Comparison between groups were made by Mann Whitney test. (E) Immunoﬂuorescence representative images showing colocalization of CCL17 with CD3 (lymphocytes), CD31 (endothelial cells) and Mac-3 (macrophages); or CCL22 with CD3, CD31, Mac-3 in VCAT. Immunoreactivity was visualized using Alexa Fluor 594 (CCL17 and CCL22, red) and Alexa Fluor 488 (CD31, CD3, Mac-3, green) secondary antibodies. Nuclei were stained with Hoechst (blue). Scale bar, 20 mm. Nuclei were stained with Hoechst (blue).

Techniques: Expressing, Comparison, MANN-WHITNEY, Staining

Prolactin Stimulates Treg Migration and CCL17 Is Important for Prolactin-Mediated Treg Recruitment. 4T1 cells were incubated in vitro in 100 ng/mL prolactin in serum-free medium for 1 h and the conditioned medium was used for the lower chamber in Transwell™ migration assays. Splenocytes from untreated Foxp3+Balb/c mice were placed in the upper Transwell™ chambers and the number of Tregs that migrated into the conditioned medium in 1 h was recorded. Conditioned medium, collected from in vitro prolactin (100 ng/mL)- stimulated 4T1 cells, was able to enhance migration of Tregs (A). Ccl17 transcripts were increased in 4T1 cells after 48 h of prolactin treatment (100 ng/mL) (B). Treatment with the selective prolactin receptor modulator, S179DPRL (100 ng/mL), by contrast, reduced expression (B). An equal volume of Dulbecco's PBS was used as the vehicle control. Treatment of 4T1 cells with 1 μM LFPRLR SMO for the same period (48 h) almost completely knocked down LF prlr without effect on mRNA for the short forms of the receptor (C). This translated to an approximately 40% reduction in LFPRLR protein, as assessed by Western blot (D). The same pretreatment with LFPRLR SMO prevented Ccl17 mRNA induction in the presence of prolactin (100 ng/mL, 48 h) compared with 1 μM Control SMO (E). 30 μM AG490, given as a 2 h pre-incubation, blocked prolactin-induced Ccl17 mRNA expression (F). Addition of CCL17 antibody into the conditioned medium derived from 1 h prolactin-stimulated 4T1 cells eliminated migration of Tregs in response to conditioned medium (G), whereas an antibody against CCL22 was without effect (H). All experiments were performed 3 times using triplicate wells on each occasion ( n = 3). For Transwell™ experiments, four independent analyses ( n = 4) were performed. Data are presented as mean ± SD. (*< p 0.05, ** < p 0.01).

Journal: Translational Oncology

Article Title: Prolactin enhances T regulatory cell promotion of breast cancer through the long form prolactin receptor

doi: 10.1016/j.tranon.2021.101195

Figure Lengend Snippet: Prolactin Stimulates Treg Migration and CCL17 Is Important for Prolactin-Mediated Treg Recruitment. 4T1 cells were incubated in vitro in 100 ng/mL prolactin in serum-free medium for 1 h and the conditioned medium was used for the lower chamber in Transwell™ migration assays. Splenocytes from untreated Foxp3+Balb/c mice were placed in the upper Transwell™ chambers and the number of Tregs that migrated into the conditioned medium in 1 h was recorded. Conditioned medium, collected from in vitro prolactin (100 ng/mL)- stimulated 4T1 cells, was able to enhance migration of Tregs (A). Ccl17 transcripts were increased in 4T1 cells after 48 h of prolactin treatment (100 ng/mL) (B). Treatment with the selective prolactin receptor modulator, S179DPRL (100 ng/mL), by contrast, reduced expression (B). An equal volume of Dulbecco's PBS was used as the vehicle control. Treatment of 4T1 cells with 1 μM LFPRLR SMO for the same period (48 h) almost completely knocked down LF prlr without effect on mRNA for the short forms of the receptor (C). This translated to an approximately 40% reduction in LFPRLR protein, as assessed by Western blot (D). The same pretreatment with LFPRLR SMO prevented Ccl17 mRNA induction in the presence of prolactin (100 ng/mL, 48 h) compared with 1 μM Control SMO (E). 30 μM AG490, given as a 2 h pre-incubation, blocked prolactin-induced Ccl17 mRNA expression (F). Addition of CCL17 antibody into the conditioned medium derived from 1 h prolactin-stimulated 4T1 cells eliminated migration of Tregs in response to conditioned medium (G), whereas an antibody against CCL22 was without effect (H). All experiments were performed 3 times using triplicate wells on each occasion ( n = 3). For Transwell™ experiments, four independent analyses ( n = 4) were performed. Data are presented as mean ± SD. (*< p 0.05, ** < p 0.01).

Article Snippet: Ten million splenocytes, isolated from Foxp3 + EGFP Balb/c mice were placed in the upper chamber (5 μm pore size, Corning 3421) and 1 mL conditioned medium from 4T1 cells with or without prolactin treatment was added to the lower chamber in the presence or absence of 1 μg/mL mouse anti-CCL17 or anti-CCL22 antibody (R & D systems, AF529, AF479, respectively).

Techniques: Migration, Incubation, In Vitro, Expressing, Control, Western Blot, Derivative Assay

RNAseq Analysis of Tumor Treg Cytokine/Chemokine Expression. RNAseq expression analysis of Tregs isolated from tumors from Control SMO- and LFPRLR SMO-treated mice showed increases (A) and decreases (B, C) in cytokine/chemokine/receptor expression. Different scales are used to more clearly illustrate the degree of change. Those in panel A not labeled and below Ccl8 in relative expression are in decreasing expression order Ccl5, Cxcl10, Il18bp, Ccl11, Cxcl13, Il21r, Il1rap, Il1r1, Tgfα, Ccl22, Cxcl9, Il24, Il5rα, Tgfβ2 , and Il22rα1 . Those decreased by LFPRLR SMO and below Il17rα in expression are in order of decreasing expression Il2rα, Il15, Cxcl11, Il15rα, Il23α, Il27rα, Il12rβ1, Ccr8, Il3rα, Il34, Cxcl15, Ccr4, Cxcr3, Il17rc and Ebi3 . Gene names are not italicized in the figure in order to increase readability. Data are the mean of 6 animals treated with Control SMO and 6 treated with LFPRLR SMO.

Journal: Translational Oncology

Article Title: Prolactin enhances T regulatory cell promotion of breast cancer through the long form prolactin receptor

doi: 10.1016/j.tranon.2021.101195

Figure Lengend Snippet: RNAseq Analysis of Tumor Treg Cytokine/Chemokine Expression. RNAseq expression analysis of Tregs isolated from tumors from Control SMO- and LFPRLR SMO-treated mice showed increases (A) and decreases (B, C) in cytokine/chemokine/receptor expression. Different scales are used to more clearly illustrate the degree of change. Those in panel A not labeled and below Ccl8 in relative expression are in decreasing expression order Ccl5, Cxcl10, Il18bp, Ccl11, Cxcl13, Il21r, Il1rap, Il1r1, Tgfα, Ccl22, Cxcl9, Il24, Il5rα, Tgfβ2 , and Il22rα1 . Those decreased by LFPRLR SMO and below Il17rα in expression are in order of decreasing expression Il2rα, Il15, Cxcl11, Il15rα, Il23α, Il27rα, Il12rβ1, Ccr8, Il3rα, Il34, Cxcl15, Ccr4, Cxcr3, Il17rc and Ebi3 . Gene names are not italicized in the figure in order to increase readability. Data are the mean of 6 animals treated with Control SMO and 6 treated with LFPRLR SMO.

Techniques: Expressing, Isolation, Control, Labeling

Review

Structured Review

Images

1) Product Images from "Macrophage-derived chemokine CCL22 establishes local LN-mediated adaptive thermogenesis and energy expenditure"

Similar Products

Image Search Results