Mus musculus
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: GSE26553MODEL2101150001
PROVIDER: PRJNA142285 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Interleukin 2 (IL-2), a cytokine linked to human autoimmune diseases, limits IL-17 production. We show that deletion of Stat3 in T cells abrogates IL-17 production and attenuates autoimmunity associated with IL-2 deficiency. While STAT3 induces IL-17 and ROR?t and inhibits Foxp3, IL-2 inhibited IL-17 independently of Foxp3 and ROR?t. We found that STAT3 and STAT5 bound to multiple common sites across the Il17 genetic locus. The induction of STAT5 binding by IL-2 was associated with a reduction in STAT3 binding at these sites and the inhibition of associated active epigenetic marks. Titrating the relative activation of STAT3 and STAT5 modulated TH17 cell specification. Thus, the balance rather than the absolute magnitude of these signals determines the propensity of cells to make a key inflammatory cytokine. The roles of STAT3 and STAT5 in regulation of gene expression under Th17 differentiation was investigated. Affymetrix Mouse Genome 430 2.0 Arrays were used to evaluate global gene expression.
2011-02-09 | E-GEOD-26551 | biostudies-arrayexpress
Project description:Genome-wide binding of STAT3 and STAT5 under Th17 conditions (ChIP-Seq)
| PRJNA142287 | ENA
Project description:Interleukin 2 (IL-2), a cytokine linked to human autoimmune diseases, limits IL-17 production. We show that deletion of Stat3 in T cells abrogates IL-17 production and attenuates autoimmunity associated with IL-2 deficiency. While STAT3 induces IL-17 and RORγt and inhibits Foxp3, IL-2 inhibited IL-17 independently of Foxp3 and RORγt. We found that STAT3 and STAT5 bound to multiple common sites across the Il17 genetic locus. The induction of STAT5 binding by IL-2 was associated with a reduction in STAT3 binding at these sites and the inhibition of associated active epigenetic marks. Titrating the relative activation of STAT3 and STAT5 modulated TH17 cell specification. Thus, the balance rather than the absolute magnitude of these signals determines the propensity of cells to make a key inflammatory cytokine. The genome-wide binding of STAT3 and STAT5 under Th17 conditions was investigated by CHIP-seq.
2011-02-09 | E-GEOD-26552 | biostudies-arrayexpress
Project description:Exosomal and cellular miRNA expression levels were measured using a microRNA chip array or quantitative reverse transcription PCR (qRT-PCR). miR-24-3p was enriched in T-EXOs from the sera of NPC patients and NPC cells, which was correlated with worse disease-free survival (DFS). Exosomes (miR-24-3p-sponge-EXO) released from miR-24-3p-sponge-TW03 cells failed to inhibit T-cell proliferation and Th1 and Th17 differentiation or to induce Treg differentiation in vitro, compared with controlNC -sponge-EXO. Mechanistic analyses revealed that in miR-24-3p-sponge-EXO-treated T-cells, P-ERK, P-STAT1 and P-STAT3 were up-regulated, whereas P-STAT5 was down-regulated compared with controlNC-sponge-EXO-treated T-cells. FGF11 was identified as a direct target gene of miR-24-3p through in vivo and in vitro assessments. More importantly, the T-EXOs repressed FGF11 expression in T-cells during proliferation and differentiation. Interestingly, when FGF11 expression in T-cells was blocked, miR-24-3p-sponge-EXOs impeded shFGF11-T-cell proliferation and Th1 and Th17 differentiation but induced Treg differentiation, like controlNC-sponge-EXO. When FGF11 was knocked down in miR-24-3p-sponge-EXO-treated T-cells, neither P-ERK, P-STAT1 and P-STAT3 up-regulation or P-STAT5 down-regulation occurred. Interestingly, FGF11 expression in tumor-infiltrating lymphocytes (TILs) was significantly and positively correlated with the number of CD4+ and CD8+ TILs and predicted favorable DFS of the patients (p < 0.05). Two-condition experiment, one nasopharyngeal carcinoma cell line TW03 vs. one normal epithelium cell line NP69. Biological replicates: 1 nasopharyngeal carcinoma cell line TW03; 1 nasopharyngeal epithelial cell line NP69.
2016-08-01 | E-GEOD-76527 | biostudies-arrayexpress
Project description: Not available
| S-EPMC8784167 | biostudies-literature
Project description:STAT3 is an immidiate regulator of Th17 differentiation. STAT3 difieciency downmodulate Th17 specific genes and Th17 responses. Therefore, we intend to identify genome wide targets of STAT3. We used microarrays to profile gene expression of STAT3 regulated genes during Th17 polarization. Total RNA was extracted from non-targeting and STAT3 siRNA treated Thp, Th0 and Th17 cell samples from different time points. Total RNA subjected to poly-A selection and hybridization on Affymetrix microarrays.
2017-05-03 | E-GEOD-67185 | biostudies-arrayexpress
Project description:Exosomal and cellular miRNA expression levels were measured using a microRNA chip array or quantitative reverse transcription PCR (qRT-PCR). miR-24-3p was enriched in T-EXOs from the sera of NPC patients and NPC cells, which was correlated with worse disease-free survival (DFS). Exosomes (miR-24-3p-sponge-EXO) released from miR-24-3p-sponge-TW03 cells failed to inhibit T-cell proliferation and Th1 and Th17 differentiation or to induce Treg differentiation in vitro, compared with controlNC -sponge-EXO. Mechanistic analyses revealed that in miR-24-3p-sponge-EXO-treated T-cells, P-ERK, P-STAT1 and P-STAT3 were up-regulated, whereas P-STAT5 was down-regulated compared with controlNC-sponge-EXO-treated T-cells. FGF11 was identified as a direct target gene of miR-24-3p through in vivo and in vitro assessments. More importantly, the T-EXOs repressed FGF11 expression in T-cells during proliferation and differentiation. Interestingly, when FGF11 expression in T-cells was blocked, miR-24-3p-sponge-EXOs impeded shFGF11-T-cell proliferation and Th1 and Th17 differentiation but induced Treg differentiation, like controlNC-sponge-EXO. When FGF11 was knocked down in miR-24-3p-sponge-EXO-treated T-cells, neither P-ERK, P-STAT1 and P-STAT3 up-regulation or P-STAT5 down-regulation occurred. Interestingly, FGF11 expression in tumor-infiltrating lymphocytes (TILs) was significantly and positively correlated with the number of CD4+ and CD8+ TILs and predicted favorable DFS of the patients (p < 0.05).
2016-08-01 | GSE76527 | GEO
Project description:Interleukin 2 (IL-2), a cytokine linked to human autoimmune diseases, limits IL-17 production. We show that deletion of Stat3 in T cells abrogates IL-17 production and attenuates autoimmunity associated with IL-2 deficiency. While STAT3 induces IL-17 and RORγt and inhibits Foxp3, IL-2 inhibited IL-17 independently of Foxp3 and RORγt. We found that STAT3 and STAT5 bound to multiple common sites across the Il17 genetic locus. The induction of STAT5 binding by IL-2 was associated with a reduction in STAT3 binding at these sites and the inhibition of associated active epigenetic marks. Titrating the relative activation of STAT3 and STAT5 modulated TH17 cell specification. Thus, the balance rather than the absolute magnitude of these signals determines the propensity of cells to make a key inflammatory cytokine.
2011-02-09 | GSE26552 | GEO
Project description:Interleukin 2 (IL-2), a cytokine linked to human autoimmune diseases, limits IL-17 production. We show that deletion of Stat3 in T cells abrogates IL-17 production and attenuates autoimmunity associated with IL-2 deficiency. While STAT3 induces IL-17 and RORγt and inhibits Foxp3, IL-2 inhibited IL-17 independently of Foxp3 and RORγt. We found that STAT3 and STAT5 bound to multiple common sites across the Il17 genetic locus. The induction of STAT5 binding by IL-2 was associated with a reduction in STAT3 binding at these sites and the inhibition of associated active epigenetic marks. Titrating the relative activation of STAT3 and STAT5 modulated TH17 cell specification. Thus, the balance rather than the absolute magnitude of these signals determines the propensity of cells to make a key inflammatory cytokine.
2011-02-09 | GSE26551 | GEO
Project description:STAT3 is an immidiate regulator of Th17 differentiation. STAT3 difieciency downmodulate Th17 specific genes and Th17 responses. Therefore, we intend to identify genome wide targets of STAT3. We used microarrays to profile gene expression of STAT3 regulated genes during Th17 polarization.
2017-05-03 | GSE67185 | GEO