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th1 and th17 cell differentiation (Takeda)

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Takeda th1 and th17 cell differentiation
Th1 And Th17 Cell Differentiation, supplied by Takeda, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 90 stars, based on 1 article reviews

th1 and th17 cell differentiation - by Bioz Stars, 2026-09

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Article Title: Laminated Layer Extract from Echinococcus Granulosus cyst Attenuates Ocular Damages and Inflammatory Responses in an Experimental Autoimmune Uveitis Model.
Article Snippet: The parasite Echinococcus granulosus is a tapeworm, which uses canids/herbivores as final hosts and omnivores as intermediate hosts.. Infection in humans is accidental through ingestion of eggs [1].. The larva of this species develops as a liquid-filled bladder bounded by a cystic wall.

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Figure 4. The expression of IL-37a can modulate the Th17/Treg ratio in CIA. (A) Determine the proportion of Th1/Th2/Th17 cells among lymph node cells by flow cytometry. And quantification of CD4+INFγ+ cells, CD4+IL4+ cells, and CD4+IL17A+ cells. NC (n = 3), WT-CIA (n = 6), IL37atg-CIA (n = 8). (B) Determination and quantification of Treg cells (CD4+FOXP3+) in lymph node cells. The positive cell population is within the black box. NC (n = 3), WT-CIA (n = 3), IL37atg-CIA (n = 4). (C) The ratio of Th1/Th2 was determined. (D) The ratio of Th17/Treg was determined. NC: the normal control was untreated wild-type mice. * p < 0.05 vs. the WT group.

Journal: International journal of molecular sciences

Article Title: IL-37 Isoform A Prevents Collagen-Induced Arthritis in Mice by Modulating the Th17/Treg Balance via IL1R8 Receptors.

doi: 10.3390/ijms252312878

Figure Lengend Snippet: Figure 4. The expression of IL-37a can modulate the Th17/Treg ratio in CIA. (A) Determine the proportion of Th1/Th2/Th17 cells among lymph node cells by flow cytometry. And quantification of CD4+INFγ+ cells, CD4+IL4+ cells, and CD4+IL17A+ cells. NC (n = 3), WT-CIA (n = 6), IL37atg-CIA (n = 8). (B) Determination and quantification of Treg cells (CD4+FOXP3+) in lymph node cells. The positive cell population is within the black box. NC (n = 3), WT-CIA (n = 3), IL37atg-CIA (n = 4). (C) The ratio of Th1/Th2 was determined. (D) The ratio of Th17/Treg was determined. NC: the normal control was untreated wild-type mice. * p < 0.05 vs. the WT group.

Article Snippet: Naïve CD4+ T cells were differentiated into Th17 cells with the assistance of the Mouse Th17 Cell Differentiation Kit (R&D Systems, Minneapolis, MN, USA).

Techniques: Expressing, Flow Cytometry, Control

Figure 5. IL-37a inhibits Th17 cell differentiation. (A) The InnateDB database was utilized to screen for DEGs associated with the innate immune response. (B) KEGG enrichment analysis of the innate immune genes regulated by IL-37a. (C) Rorc mRNA expression in single-cell suspensions from draining LNs was measured by qPCR, and the NCs were not used to treat the WT mice (n = 3). (D) Flow cytometry and quantification of CD4+IL17+ cells among sorted naïve T cells from WT mice and IL-37atg mice under Th17-polarizing conditions. The positive cell population is within the black box. WT (n = 4), IL37atg (n = 4). * p < 0.05 and ** p < 0.01 vs. the WT group.

Journal: International journal of molecular sciences

Article Title: IL-37 Isoform A Prevents Collagen-Induced Arthritis in Mice by Modulating the Th17/Treg Balance via IL1R8 Receptors.

doi: 10.3390/ijms252312878

Figure Lengend Snippet: Figure 5. IL-37a inhibits Th17 cell differentiation. (A) The InnateDB database was utilized to screen for DEGs associated with the innate immune response. (B) KEGG enrichment analysis of the innate immune genes regulated by IL-37a. (C) Rorc mRNA expression in single-cell suspensions from draining LNs was measured by qPCR, and the NCs were not used to treat the WT mice (n = 3). (D) Flow cytometry and quantification of CD4+IL17+ cells among sorted naïve T cells from WT mice and IL-37atg mice under Th17-polarizing conditions. The positive cell population is within the black box. WT (n = 4), IL37atg (n = 4). * p < 0.05 and ** p < 0.01 vs. the WT group.

Article Snippet: Naïve CD4+ T cells were differentiated into Th17 cells with the assistance of the Mouse Th17 Cell Differentiation Kit (R&D Systems, Minneapolis, MN, USA).

Techniques: Cell Differentiation, Expressing, Flow Cytometry

Fig. 1 STAT3 and SOX-5 activate RORCE2 in Th17 cells. a The deletion of the STAT3-BS sequence in RORCE2 by CRISPR/Cas9 (top) and conﬁrmation by sequencing (bottom). b–d ChIP‒qPCR assays were performed on WT and STAT3-BS−/−Th17-polarized cells with the indicated antibodies. e ChIP‒qPCR was performed on WT and SOX-5-BS−/−Th17-polarized cells with the indicated antibodies. STAT3-SOX-5-BS indicates the location covering the STAT3 binding site and SOX-5 binding site in RORCE2. CNS9 (+5802 to +7963 bp from the RORC TSS) indicates a cis-regulatory element distal to STAT3-BS in RORCE2 and can be bound by STAT3, as the negative control for ChIP‒qPCR in this study. f, g 3C-qPCR (f) and ChIP-loop assays (with an anti-STAT3 antibody) (g) were performed to evaluate the interaction between RORCE2 and the RORγt gene promoter in WT and STAT3-BS−/−Th17-polarized cells. Means ± SEMs are shown, n = 5 biologically independent animals (b–e), n = 3 biologically independent animals (f, g). D = differentiation.

Journal: Communications biology

Article Title: STAT3 and SOX-5 induce BRG1-mediated chromatin remodeling of RORCE2 in Th17 cells.

doi: 10.1038/s42003-023-05735-9

Figure Lengend Snippet: Fig. 1 STAT3 and SOX-5 activate RORCE2 in Th17 cells. a The deletion of the STAT3-BS sequence in RORCE2 by CRISPR/Cas9 (top) and conﬁrmation by sequencing (bottom). b–d ChIP‒qPCR assays were performed on WT and STAT3-BS−/−Th17-polarized cells with the indicated antibodies. e ChIP‒qPCR was performed on WT and SOX-5-BS−/−Th17-polarized cells with the indicated antibodies. STAT3-SOX-5-BS indicates the location covering the STAT3 binding site and SOX-5 binding site in RORCE2. CNS9 (+5802 to +7963 bp from the RORC TSS) indicates a cis-regulatory element distal to STAT3-BS in RORCE2 and can be bound by STAT3, as the negative control for ChIP‒qPCR in this study. f, g 3C-qPCR (f) and ChIP-loop assays (with an anti-STAT3 antibody) (g) were performed to evaluate the interaction between RORCE2 and the RORγt gene promoter in WT and STAT3-BS−/−Th17-polarized cells. Means ± SEMs are shown, n = 5 biologically independent animals (b–e), n = 3 biologically independent animals (f, g). D = differentiation.

Article Snippet: Th17, Th1 and Th2 polarizations were then conducted following the instructions of the CellXVivo mouse Th17 cell differentiation kit (R&D Systems, CDK017), the CellXVivo mouse Th1 cell differentiation kit (R&D Systems, CDK018) and the CellXVivo mouse Th2 cell differentiation kit (R&D Systems, CDK019), respectively.

Techniques: Sequencing, CRISPR, Binding Assay, Negative Control

Fig. 2 STAT3-BS deﬁciency of RORCE2 downregulates RORγt expression and Th17 cell differentiation in vivo. a The relative mRNA levels of RORγt in CD4+ T cells from the spleens of WT and STAT3-BS−/−mice were quantiﬁed by RT‒qPCR. b, c RORγt+ Th17 cell frequency in splenic CD4+ T cells from WT and STAT3-BS−/−mice and mean ﬂuorescence intensity (MFI) of RORγt in RORγt+ Th17 cells were analyzed by ﬂow cytometry (b) and statistically evaluated (c). d The relative mRNA levels of IL-17A in CD4+ T cells from the spleens of the WT and STAT3-BS−/−mice. e, f IL-17A+ Th17 cell frequencies among splenic CD4+ T cells of the WT and STAT3-BS−/−mice. g, h RORγt+ Th17 cell frequencies among CD4+ CD45+ Lin+ T cells were determined by ﬂow cytometry in LPLs of the small intestine from the WT and STAT3-BS−/−mice and RORγt MFI in Th17 cells. i, j IL-17A+ Th17 cell frequencies among CD4+ CD45+ Lin+ T cells from LPLs of the small intestine from the WT and STAT3-BS−/−mice. Means ± SEMs are shown, n = 5 biologically independent animals (a, c, d, f), n = 3 biologically independent animals (h, j).

Journal: Communications biology

Article Title: STAT3 and SOX-5 induce BRG1-mediated chromatin remodeling of RORCE2 in Th17 cells.

doi: 10.1038/s42003-023-05735-9

Figure Lengend Snippet: Fig. 2 STAT3-BS deﬁciency of RORCE2 downregulates RORγt expression and Th17 cell differentiation in vivo. a The relative mRNA levels of RORγt in CD4+ T cells from the spleens of WT and STAT3-BS−/−mice were quantiﬁed by RT‒qPCR. b, c RORγt+ Th17 cell frequency in splenic CD4+ T cells from WT and STAT3-BS−/−mice and mean ﬂuorescence intensity (MFI) of RORγt in RORγt+ Th17 cells were analyzed by ﬂow cytometry (b) and statistically evaluated (c). d The relative mRNA levels of IL-17A in CD4+ T cells from the spleens of the WT and STAT3-BS−/−mice. e, f IL-17A+ Th17 cell frequencies among splenic CD4+ T cells of the WT and STAT3-BS−/−mice. g, h RORγt+ Th17 cell frequencies among CD4+ CD45+ Lin+ T cells were determined by ﬂow cytometry in LPLs of the small intestine from the WT and STAT3-BS−/−mice and RORγt MFI in Th17 cells. i, j IL-17A+ Th17 cell frequencies among CD4+ CD45+ Lin+ T cells from LPLs of the small intestine from the WT and STAT3-BS−/−mice. Means ± SEMs are shown, n = 5 biologically independent animals (a, c, d, f), n = 3 biologically independent animals (h, j).

Techniques: Expressing, Cell Differentiation, In Vivo, Cytometry

Fig. 3 STAT3-BS deﬁciency of RORCE2 results in impaired Th17 cell polarization in vitro. Naïve CD4+ T cells from the spleens of WT or STAT3-BS−/−

Journal: Communications biology

Article Title: STAT3 and SOX-5 induce BRG1-mediated chromatin remodeling of RORCE2 in Th17 cells.

doi: 10.1038/s42003-023-05735-9

Figure Lengend Snippet: Fig. 3 STAT3-BS deﬁciency of RORCE2 results in impaired Th17 cell polarization in vitro. Naïve CD4+ T cells from the spleens of WT or STAT3-BS−/−

Techniques: In Vitro

Fig. 4 STAT3-BS deﬁciency in RORCE2 alleviates the severity of EAE. a The mean daily clinical scores of EAE for WT and STAT3-BS−/−mice are shown. b Representative staining image of hematoxylin-eosin (HE) and luxol fast blue (LFB) in the spinal cord sections at 30 days after immunization. Scale bars, 500 or 100 µm. c–e Flow cytometry analysis of mononuclear cells from the spinal cord of EAE-induced WT and STAT3-BS−/−mice at 30 days after immunization. Th17 cell frequencies among CD4+ T cells (c, d). The numbers of inﬁltrating CD4+ T cells in the spinal cord (e). f Inguinal lymph node cells were extracted at day 8 after immunization and restimulation with MOG peptide for 3 days. IL-17A, IFNγ, and IL-4 production were examined by ELISA. Means ± SEMs are shown, n = 5 biologically independent animals (d, f), n = 3 biologically independent animals (e).

Journal: Communications biology

Article Title: STAT3 and SOX-5 induce BRG1-mediated chromatin remodeling of RORCE2 in Th17 cells.

doi: 10.1038/s42003-023-05735-9

Figure Lengend Snippet: Fig. 4 STAT3-BS deﬁciency in RORCE2 alleviates the severity of EAE. a The mean daily clinical scores of EAE for WT and STAT3-BS−/−mice are shown. b Representative staining image of hematoxylin-eosin (HE) and luxol fast blue (LFB) in the spinal cord sections at 30 days after immunization. Scale bars, 500 or 100 µm. c–e Flow cytometry analysis of mononuclear cells from the spinal cord of EAE-induced WT and STAT3-BS−/−mice at 30 days after immunization. Th17 cell frequencies among CD4+ T cells (c, d). The numbers of inﬁltrating CD4+ T cells in the spinal cord (e). f Inguinal lymph node cells were extracted at day 8 after immunization and restimulation with MOG peptide for 3 days. IL-17A, IFNγ, and IL-4 production were examined by ELISA. Means ± SEMs are shown, n = 5 biologically independent animals (d, f), n = 3 biologically independent animals (e).

Techniques: Staining, Flow Cytometry, Enzyme-linked Immunosorbent Assay

Fig. 5 The binding of STAT3 and SOX-5 on RORCE2 is essential for the recruitment of BRG1. a ATAC-seq data at the RORC locus in STAT3ﬂ/ﬂTh17 cells versus STAT3ﬂ/ﬂ-CD4Cre Th17 cells. b A chromatin accessibility assay was performed on SOX-5-BS and STAT3-BS in RORCE2 in the WT and STAT3-BS−/−Th17-polarized cells. c The expression of BRG1 and GAPDH proteins in the WT, STAT3-BS−/−and SOX-5-BS−/−Th17-polarized cells was detected by Western blotting. d, e ChIP‒qPCR assays of BRG1 were performed in the WT, STAT3-BS−/−and SOX-5-BS−/−Th17-polarized cells. CNS9 (+5802 to +7963 bp from the RORC TSS) indicates a cis-regulatory element distal to STAT3-BS in RORCE2 and can be bound by STAT3, as the negative control for ChIP‒qPCR in this study. f Transfected HeLa cells were subjected to IP with the indicated antibody. Input and IP proteins were then subjected to IB with the indicated antibody. g Whole-cell lysates from Th17 cells were subjected to IP with an anti-BRG1 antibody or control mouse IgG and to IB with an anti-STAT3 or anti-SOX-5 antibody. Input proteins (input) were also subjected to IB with an anti-STAT3 or anti-SOX-5 antibody. Means ± SEMs are shown, n = 5 biologically independent animals (b, d, e). D = differentiation.

Journal: Communications biology

Article Title: STAT3 and SOX-5 induce BRG1-mediated chromatin remodeling of RORCE2 in Th17 cells.

doi: 10.1038/s42003-023-05735-9

Figure Lengend Snippet: Fig. 5 The binding of STAT3 and SOX-5 on RORCE2 is essential for the recruitment of BRG1. a ATAC-seq data at the RORC locus in STAT3ﬂ/ﬂTh17 cells versus STAT3ﬂ/ﬂ-CD4Cre Th17 cells. b A chromatin accessibility assay was performed on SOX-5-BS and STAT3-BS in RORCE2 in the WT and STAT3-BS−/−Th17-polarized cells. c The expression of BRG1 and GAPDH proteins in the WT, STAT3-BS−/−and SOX-5-BS−/−Th17-polarized cells was detected by Western blotting. d, e ChIP‒qPCR assays of BRG1 were performed in the WT, STAT3-BS−/−and SOX-5-BS−/−Th17-polarized cells. CNS9 (+5802 to +7963 bp from the RORC TSS) indicates a cis-regulatory element distal to STAT3-BS in RORCE2 and can be bound by STAT3, as the negative control for ChIP‒qPCR in this study. f Transfected HeLa cells were subjected to IP with the indicated antibody. Input and IP proteins were then subjected to IB with the indicated antibody. g Whole-cell lysates from Th17 cells were subjected to IP with an anti-BRG1 antibody or control mouse IgG and to IB with an anti-STAT3 or anti-SOX-5 antibody. Input proteins (input) were also subjected to IB with an anti-STAT3 or anti-SOX-5 antibody. Means ± SEMs are shown, n = 5 biologically independent animals (b, d, e). D = differentiation.

Techniques: Binding Assay, Expressing, Western Blot, Negative Control, Transfection, Control

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