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th17 23 condition (R&D Systems)

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R&D Systems th17 23 condition
FIGURE 4. <t>Th17</t> cell–intrinsic miR-22 deletion exacerbates autoimmune EAE.

Th17 23 Condition, supplied by R&D Systems, used in various techniques. Bioz Stars score: 96/100, based on 333 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/th17 23 condition/product/R&D Systems
Average 96 stars, based on 333 article reviews

th17 23 condition - by Bioz Stars, 2026-04

96/100 stars

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1) Product Images from "The MicroRNA miR-22 Represses Th17 Cell Pathogenicity by Targeting PTEN-Regulated Pathways."

Article Title: The MicroRNA miR-22 Represses Th17 Cell Pathogenicity by Targeting PTEN-Regulated Pathways.

Journal: ImmunoHorizons

doi: 10.4049/immunohorizons.2000008

Figure Legend Snippet: FIGURE 4. Th17 cell–intrinsic miR-22 deletion exacerbates autoimmune EAE.

Techniques Used:

Figure Legend Snippet: FIGURE 5. miR-22 represses Th17 cell pathogenicity by targeting PTEN-regulated pathway. (A) Expression profile of pathogenicity signature genes of the pathogenic Th17 cells from control and miR-222/2 are measured by qRT-PCR. Data

Techniques Used: Expressing, Control, Quantitative RT-PCR

Image Search Results

In murine, splenic CD4+ T cells, elevated O-GlcNAcylation increases pro-inflammatory IL-17A transcript and protein levels. A, TMG treatment increases O-GlcNAc levels over the course of splenic CD4+ T cell population differentiation and proliferation with corresponding decreases in OGT and increases in OGA. The red arrow indicates the time of restimulation. The blot is representative of three experiments. B, protein levels of cytokines secreted from splenic, total CD4+ T cells with or without TMG treatment. C, transcript levels of cytokines secreted from splenic, total CD4+ T cells with or without TMG treatment. D, O-GlcNAc levels remain elevated in Th17-polarized splenic CD4+ T cells on day 4 and normalize following 24 h of restimulation (day 5). The blot is representative of three experiments. E, protein level of IL-17A secreted by splenic naive CD4+ T cells polarized to Th17 lineage treated with or without TMG. F, transcript level of IL-17A secreted by splenic, naive CD4+ T cells polarized to Th17 lineage treated with or without TMG. G, frequency of live CD4+ IL-17+ cells is significantly increased with TMG treatment. 25,000 cells were analyzed per condition. Dead cells were excluded. A representative histogram is shown in Fig. S1. Bars, mean ± S.E. (error bars) of five biological replicates in B and C and four different biological replicates in E–G. Bars, median ± S.E. (error bars) of four biological replicates in G; *, p < 0.05; ***, p < 0.001.

Journal: The Journal of Biological Chemistry

Article Title: Elevated O -GlcNAcylation enhances pro-inflammatory Th17 function by altering the intracellular lipid microenvironment

doi: 10.1074/jbc.RA119.008373

Figure Lengend Snippet: In murine, splenic CD4+ T cells, elevated O-GlcNAcylation increases pro-inflammatory IL-17A transcript and protein levels. A, TMG treatment increases O-GlcNAc levels over the course of splenic CD4+ T cell population differentiation and proliferation with corresponding decreases in OGT and increases in OGA. The red arrow indicates the time of restimulation. The blot is representative of three experiments. B, protein levels of cytokines secreted from splenic, total CD4+ T cells with or without TMG treatment. C, transcript levels of cytokines secreted from splenic, total CD4+ T cells with or without TMG treatment. D, O-GlcNAc levels remain elevated in Th17-polarized splenic CD4+ T cells on day 4 and normalize following 24 h of restimulation (day 5). The blot is representative of three experiments. E, protein level of IL-17A secreted by splenic naive CD4+ T cells polarized to Th17 lineage treated with or without TMG. F, transcript level of IL-17A secreted by splenic, naive CD4+ T cells polarized to Th17 lineage treated with or without TMG. G, frequency of live CD4+ IL-17+ cells is significantly increased with TMG treatment. 25,000 cells were analyzed per condition. Dead cells were excluded. A representative histogram is shown in Fig. S1. Bars, mean ± S.E. (error bars) of five biological replicates in B and C and four different biological replicates in E–G. Bars, median ± S.E. (error bars) of four biological replicates in G; *, p < 0.05; ***, p < 0.001.

Article Snippet: CD4 + T cells were cultured under Th17 conditions (human IL-6 (50 ng/ml), human IL-1β (10 ng/ml), human IL-23 (10 ng/ml), human TGFβ1 (3 ng/ml) (all Miltenyi), and neutralizing antibodies to IFNγ (clone: XMG1.2) and IL-4 (clone: 11B11) at 10 μg/ml (Bio X Cell)).

Techniques:

In human CD4+ T cells isolated from peripheral blood, elevated O-GlcNAcylation increases pro-inflammatory IL-17A transcript and cytokine levels. A, clinical characteristics of human blood donors. B, TMG treatment increases IL-17A secretion from total human CD4+ cells isolated from peripheral blood and polarized under Th17 conditions. C, IL-17, IL-23R, and IFNγ transcript levels all significantly increase with TMG treatment. Bars, mean ± S.E. (error bars) of 9 and 7 human donors in B and C, respectively. *, p < 0.05; **, p < 0.01. BMI, body mass index.

Journal: The Journal of Biological Chemistry

Article Title: Elevated O -GlcNAcylation enhances pro-inflammatory Th17 function by altering the intracellular lipid microenvironment

doi: 10.1074/jbc.RA119.008373

Figure Lengend Snippet: In human CD4+ T cells isolated from peripheral blood, elevated O-GlcNAcylation increases pro-inflammatory IL-17A transcript and cytokine levels. A, clinical characteristics of human blood donors. B, TMG treatment increases IL-17A secretion from total human CD4+ cells isolated from peripheral blood and polarized under Th17 conditions. C, IL-17, IL-23R, and IFNγ transcript levels all significantly increase with TMG treatment. Bars, mean ± S.E. (error bars) of 9 and 7 human donors in B and C, respectively. *, p < 0.05; **, p < 0.01. BMI, body mass index.

Techniques: Isolation

Western diet feeding in mice results in elevated O-GlcNAc levels in splenic, naive CD4+ T cells and increases IL-17A secretion from splenic, naive CD4+ T cells, which is exacerbated by TMG treatment. A, WD feeding results in significantly increased weight gain. B, WD feeding results in significantly elevated fasting blood glucose levels. C, WD-fed mice have significantly elevated O-GlcNAc levels. D, splenic, naive CD4+ T cells polarized to the Th17 lineage from WD-fed mice secrete significantly more IL-17A than cells from SC mice. Cells from SC-fed mice treated with TMG secrete levels similar to cells from WD mice, and TMG treatment of cells from WD-fed mice significantly exacerbates IL-17A secretion. E, IL-17A transcript levels mimic the trends seen with IL-17A protein secretion. In A and B, points represent average ± S.D. (error bars) and are calculated from four and five biological replicates (SC and WD, respectively). In C, the graph of densitometry is from eight biological replicates, and bars represent mean ± S.D. (error bars). Each lane in the blot represents whole-cell lysate from one mouse. In D and E, bars represent mean ± S.E. (error bars) of four and five biological replicates (SC and WD, respectively). HPRT is used an internal reference for gene expression. *, p < 0.05; **, p < 0.01; ***, p < 0.001.

Journal: The Journal of Biological Chemistry

Article Title: Elevated O -GlcNAcylation enhances pro-inflammatory Th17 function by altering the intracellular lipid microenvironment

doi: 10.1074/jbc.RA119.008373

Figure Lengend Snippet: Western diet feeding in mice results in elevated O-GlcNAc levels in splenic, naive CD4+ T cells and increases IL-17A secretion from splenic, naive CD4+ T cells, which is exacerbated by TMG treatment. A, WD feeding results in significantly increased weight gain. B, WD feeding results in significantly elevated fasting blood glucose levels. C, WD-fed mice have significantly elevated O-GlcNAc levels. D, splenic, naive CD4+ T cells polarized to the Th17 lineage from WD-fed mice secrete significantly more IL-17A than cells from SC mice. Cells from SC-fed mice treated with TMG secrete levels similar to cells from WD mice, and TMG treatment of cells from WD-fed mice significantly exacerbates IL-17A secretion. E, IL-17A transcript levels mimic the trends seen with IL-17A protein secretion. In A and B, points represent average ± S.D. (error bars) and are calculated from four and five biological replicates (SC and WD, respectively). In C, the graph of densitometry is from eight biological replicates, and bars represent mean ± S.D. (error bars). Each lane in the blot represents whole-cell lysate from one mouse. In D and E, bars represent mean ± S.E. (error bars) of four and five biological replicates (SC and WD, respectively). HPRT is used an internal reference for gene expression. *, p < 0.05; **, p < 0.01; ***, p < 0.001.

Techniques: Western Blot, Expressing

Elevated O-GlcNAcylation has no effect on RORγt protein or transcript levels but does promote retention of RORγt at the IL-17 locus. A, splenic, naive CD4+ T cells were polarized to the Th17 lineage with and without TMG and cultured for 4 days. Prior to restimulation on the fourth day of culture (0) and over 24 h after restimulation, RORγt protein levels were unchanged. Densitometry was used to compare the RORγt/actin ratio at specified time points. The blot is representative of three biological replicates. Densitometry bars represent the mean ± S.E. (error bars) of three biological replicates. B, transcript levels of RORγt are unchanged 24 h after restimulation. RORγt gene expression was normalized to HPRT expression. Bars, mean ± S.E. (error bars) of five biological replicates. C, TMG treatment significantly increases RORγt binding at the IL-17 promoter and CNS2 enhancer regions in ChIP assays. Bars, mean ± S.E. (error bars) of four biological replicates. *, p < 0.05; **, p < 0.01.

Journal: The Journal of Biological Chemistry

Article Title: Elevated O -GlcNAcylation enhances pro-inflammatory Th17 function by altering the intracellular lipid microenvironment

doi: 10.1074/jbc.RA119.008373

Figure Lengend Snippet: Elevated O-GlcNAcylation has no effect on RORγt protein or transcript levels but does promote retention of RORγt at the IL-17 locus. A, splenic, naive CD4+ T cells were polarized to the Th17 lineage with and without TMG and cultured for 4 days. Prior to restimulation on the fourth day of culture (0) and over 24 h after restimulation, RORγt protein levels were unchanged. Densitometry was used to compare the RORγt/actin ratio at specified time points. The blot is representative of three biological replicates. Densitometry bars represent the mean ± S.E. (error bars) of three biological replicates. B, transcript levels of RORγt are unchanged 24 h after restimulation. RORγt gene expression was normalized to HPRT expression. Bars, mean ± S.E. (error bars) of five biological replicates. C, TMG treatment significantly increases RORγt binding at the IL-17 promoter and CNS2 enhancer regions in ChIP assays. Bars, mean ± S.E. (error bars) of four biological replicates. *, p < 0.05; **, p < 0.01.

Techniques: Cell Culture, Expressing, Binding Assay

In murine, Th17-differentiated cells, elevated O-GlcNAc increases lipid ligands capable of increasing RORγt transcriptional activity. A, splenic, naive CD4+ T cells were polarized to the Th17 lineage with and without TMG and cultured for 4 days and then restimulated for 8 h before harvesting for lipid analysis. The absolute value or normalized ion abundance of total sterols and cholesterol is increased with TMG treatment. B, of the top 20 fatty acids present in cells, the percentage of saturated fatty acids increased with TMG treatment. C, of the top 20 fatty acids present in cells, the percentage of polyunsaturated fatty acids decreased with TMG treatment. D, choline was shunted away from phosphatidylcholine and sphingomyelin synthesis, leading to a rise in ceramide levels. Bars, mean ± S.D. (error bars) of five biological replicates. *, p < 0.05; **, p < 0.01; ***, p < 0.001. PE, phosphatidylethanolamine; PG, phosphatidylglycerol; PI, phosphatidylinositol; PS, phosphatidylserine.

Journal: The Journal of Biological Chemistry

Article Title: Elevated O -GlcNAcylation enhances pro-inflammatory Th17 function by altering the intracellular lipid microenvironment

doi: 10.1074/jbc.RA119.008373

Figure Lengend Snippet: In murine, Th17-differentiated cells, elevated O-GlcNAc increases lipid ligands capable of increasing RORγt transcriptional activity. A, splenic, naive CD4+ T cells were polarized to the Th17 lineage with and without TMG and cultured for 4 days and then restimulated for 8 h before harvesting for lipid analysis. The absolute value or normalized ion abundance of total sterols and cholesterol is increased with TMG treatment. B, of the top 20 fatty acids present in cells, the percentage of saturated fatty acids increased with TMG treatment. C, of the top 20 fatty acids present in cells, the percentage of polyunsaturated fatty acids decreased with TMG treatment. D, choline was shunted away from phosphatidylcholine and sphingomyelin synthesis, leading to a rise in ceramide levels. Bars, mean ± S.D. (error bars) of five biological replicates. *, p < 0.05; **, p < 0.01; ***, p < 0.001. PE, phosphatidylethanolamine; PG, phosphatidylglycerol; PI, phosphatidylinositol; PS, phosphatidylserine.

Techniques: Activity Assay, Cell Culture

ACC1 is modified by O-GlcNAc. A, splenic, naive CD4+ T cells were polarized to the Th17 lineage with and without TMG and cultured for 4 days before restimulation for 24 h. Inhibitory phosphorylation of ACC1 at Ser-79 is unchanged with TMG treatment over the 24 h of restimulation. pACC1 and ACC1 levels were normalized to actin. Blot is representative of three biological replicates. Densitometry bars, mean ± S.E. (error bars) of three replicates. B, ACC1 or O-GlcNAc–modified proteins were immunoprecipitated (IP) from splenic CD4+ T cells and show that ACC1 is modified by O-GlcNAc. Blots are representative of three biological replicates each. C, representative mass spectra plot of high confidence O-GlcNAc–modified sites Ser-966 and Ser-976 on an ACC1 peptide. D, location of analogous O-GlcNAc–modified residues Ser-2129 and Ser-2323 in the carboxyl transferase domain on a purified human partial C-terminal crystal structure of ACC1 (Protein Data Bank entry 4ASI). E, palmitic acid significantly decreases with TMG treatment. Bars, mean ± S.D. (error bars) of five replicates; **, p < 0.01.

Journal: The Journal of Biological Chemistry

Article Title: Elevated O -GlcNAcylation enhances pro-inflammatory Th17 function by altering the intracellular lipid microenvironment

doi: 10.1074/jbc.RA119.008373

Figure Lengend Snippet: ACC1 is modified by O-GlcNAc. A, splenic, naive CD4+ T cells were polarized to the Th17 lineage with and without TMG and cultured for 4 days before restimulation for 24 h. Inhibitory phosphorylation of ACC1 at Ser-79 is unchanged with TMG treatment over the 24 h of restimulation. pACC1 and ACC1 levels were normalized to actin. Blot is representative of three biological replicates. Densitometry bars, mean ± S.E. (error bars) of three replicates. B, ACC1 or O-GlcNAc–modified proteins were immunoprecipitated (IP) from splenic CD4+ T cells and show that ACC1 is modified by O-GlcNAc. Blots are representative of three biological replicates each. C, representative mass spectra plot of high confidence O-GlcNAc–modified sites Ser-966 and Ser-976 on an ACC1 peptide. D, location of analogous O-GlcNAc–modified residues Ser-2129 and Ser-2323 in the carboxyl transferase domain on a purified human partial C-terminal crystal structure of ACC1 (Protein Data Bank entry 4ASI). E, palmitic acid significantly decreases with TMG treatment. Bars, mean ± S.D. (error bars) of five replicates; **, p < 0.01.

Techniques: Modification, Cell Culture, Immunoprecipitation, Purification

O-GlcNAc regulates pro-inflammatory Th17 cell function. This schematic represents diet-induced changes in O-GlcNAc levels leading to increased ACC1 O-GlcNAcylation and alterations in the lipidome. Changes in lipid expression activate RORγt, leading to more IL-17 production.

Journal: The Journal of Biological Chemistry

Article Title: Elevated O -GlcNAcylation enhances pro-inflammatory Th17 function by altering the intracellular lipid microenvironment

doi: 10.1074/jbc.RA119.008373

Figure Lengend Snippet: O-GlcNAc regulates pro-inflammatory Th17 cell function. This schematic represents diet-induced changes in O-GlcNAc levels leading to increased ACC1 O-GlcNAcylation and alterations in the lipidome. Changes in lipid expression activate RORγt, leading to more IL-17 production.

Techniques: Cell Function Assay, Expressing

Journal: ImmunoHorizons

Article Title: The MicroRNA miR-22 Represses Th17 Cell Pathogenicity by Targeting PTEN-Regulated Pathways.

doi: 10.4049/immunohorizons.2000008

Figure Lengend Snippet: FIGURE 4. Th17 cell–intrinsic miR-22 deletion exacerbates autoimmune EAE.

Article Snippet: The following conditions were used: Th17 (b) condition (catalog no. 7666-MB-005, 2 ng/ml TGF-b1 [R&D Systems]; catalog no. 406-ML-025, 20 ng/ml IL-6 [R&DSystems]; catalog no. 16-7041- 95, 10mg/ml anti–IL-4mAb [ThermoFisher]; and catalog no. 16- 7311-38, 10 mg/ml anti–IFN-gmAb [Thermo Fisher Scientific]), Th17 (23) condition (catalog no. 406-ML-025, 20 ng/ml IL-6 [R&D Systems]; catalog no. 401-ML-025, 20 ng/ml IL-1b [R&D Systems]; catalogno.

Techniques:

Journal: ImmunoHorizons

Article Title: The MicroRNA miR-22 Represses Th17 Cell Pathogenicity by Targeting PTEN-Regulated Pathways.

doi: 10.4049/immunohorizons.2000008

Figure Lengend Snippet: FIGURE 5. miR-22 represses Th17 cell pathogenicity by targeting PTEN-regulated pathway. (A) Expression profile of pathogenicity signature genes of the pathogenic Th17 cells from control and miR-222/2 are measured by qRT-PCR. Data

Techniques: Expressing, Control, Quantitative RT-PCR

Journal: ImmunoHorizons

Article Title: The MicroRNA miR-22 Represses Th17 Cell Pathogenicity by Targeting PTEN-Regulated Pathways.

doi: 10.4049/immunohorizons.2000008

Figure Lengend Snippet: FIGURE 4. Th17 cell–intrinsic miR-22 deletion exacerbates autoimmune EAE.

Techniques:

Journal: ImmunoHorizons

Article Title: The MicroRNA miR-22 Represses Th17 Cell Pathogenicity by Targeting PTEN-Regulated Pathways.

doi: 10.4049/immunohorizons.2000008

Techniques: Expressing, Control, Quantitative RT-PCR

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1) Product Images from "The MicroRNA miR-22 Represses Th17 Cell Pathogenicity by Targeting PTEN-Regulated Pathways."

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