Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

TCR signaling induces STAT3 phosphorylation to promote TH17 cell differentiation

ABSTRACT: To systematically evaluate the effect of inhibition of Lck/Fyn kinase activity on the differentiation of TH17 and Treg cells.

ORGANISM(S): Mus musculus

PROVIDER: GSE229377 | GEO | 2024/01/31

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

TCR signaling induces STAT3 phosphorylation to promote TH17 cell differentiation.

Project description:TH17 differentiation is critically controlled by "signal 3" of cytokines (IL-6/IL-23) through STAT3. However, cytokines alone induced only a moderate level of STAT3 phosphorylation. Surprisingly, TCR stimulation alone induced STAT3 phosphorylation through Lck/Fyn, and synergistically with IL-6/IL-23 induced robust and optimal STAT3 phosphorylation at Y705. Inhibition of Lck/Fyn kinase activity by Srci1 or disrupting the interaction between Lck/Fyn and STAT3 by disease-causing STAT3 mutations selectively impaired TCR stimulation, but not cytokine-induced STAT3 phosphorylation, which consequently abolished TH17 differentiation and converted them to FOXP3+ Treg cells. Srci1 administration or disrupting the interaction between Lck/Fyn and STAT3 significantly ameliorated TH17 cell-mediated EAE disease. These findings uncover an unexpected deterministic role of TCR signaling in fate determination between TH17 and Treg cells through Lck/Fyn-dependent phosphorylation of STAT3, which can be exploited to develop therapeutics selectively against TH17-related autoimmune diseases. Our study thus provides insight into how TCR signaling could integrate with cytokine signal to direct T cell differentiation.

| S-EPMC10849914 | biostudies-literature

TCR signaling induces STAT3 phosphorylation to promote TH17 cell differentiation

Project description:TCR signaling induces STAT3 phosphorylation to promote TH17 cell differentiation

| PRJNA954300 | ENA

Role of Stat3 phosphorylation in Th17 differentiation

Project description:Determine the role of stat3 phosphorylation, particularly at S727, during the differentiation of Th17 cells.

2025-10-29 | PXD059588 | Pride

Investigating the role of STAT3 in Th17 differentiation

Project description:Our lab is working to understand the role of STAT3 and the phosphorylation at S727 in Th17 cell differentiation

2025-10-29 | PXD065517 | Pride

LCK-deficient CD8 T-cell show reduced proliferation but normal effector responses in vivo

Project description:The overall study investigated the role of LCK and FYN in peripheral CD8⁺ T-cell responses using adoptive transfers of LCK- or FYN-deficient monoclonal T cells into polyclonal hosts. To assess the role of LCK in T-cell differentiation in greater detail, we performed a single-cell transcriptomics study of WT, LCK CA (knock-in mice with LCK unable to bind to CD4/CD8 co-receptors), and LCK KO OT-I CD8⁺ T cells responding to LM-OVA on day 5 post-infection. While the WT and LCK CA T cells were indistinguishable, LCK KO T cells exhibited a higher frequency of effector T cells and a lower frequency of memory T cells compared to the controls.

2025-08-15 | GSE304760 | GEO

Mitochondrial proteomics of Th17 and Treg cells

Project description:After treatment with NCA029 under DSS, Th17 and Treg cells were collected, and mitochondria were extracted for proteomic analysis.

2024-10-16 | PXD056878 |

PTEN-induced kinase 1 (PINK1) ameliorates autoimmune disease via negative regulation of the STAT3-Th17 axis

Project description:Th17-related genes increased in T cells from PINK1-deficient mice. Th17 and Treg cells were increased and decreased in PINK1-deficient cells, respectively, and phosphorylation of signal transducer and activator of transcription 3 (STAT3) was increased in PINK1-deficient cells.

2024-01-29 | GSE254099 | GEO

Expression data from Th17 cells of different origins

Project description:Foxp3 is indispensable for Treg suppressive function, but the stability of Foxp3 has been controversial. In autoimmune arthritis, Th17 cells play a critically important pathological role, but the origin of Th17 cells remains unknown We used microarrays to detail the global programme of gene expression of Th17 cells originated from Foxp3+T cells compared to conventional naive CD4+T cells derived Th17 cells. We also take samples of Treg cells and Th0 cells for the experimetnatl control. Each T cell subset after the culture was subjected to RNA extraction and hybridization on Affymetrix microarrays.

2013-12-21 | E-GEOD-48428 | biostudies-arrayexpress

The effect of dexmedetomidine on perioperative cholinergic anti-inflammatory pathway and the balance of Th17 / Treg in colorectal cancer patients

Project description:Interventions: DEX: a loading dosage of dexmedetomidine (0.5 ug/Kg) was infused introvenously 10 min before anesthesia and followed continously at0.5 ug/Kg/h for 2h;control:saline Primary outcome(s): interleukin-17, 6, 23, 10, 1ß, TNF-a, TGFß-1, HMGB1, Th17/Treg cell count Study Design: Randomized parallel controlled trial

| 2663054 | ecrin-mdr-crc

Human chorionic gonadotropin promotes murine Treg cells and restricts pregnancy-harmful proinflammatory Th17 responses – proteomics data

Project description:In this study, the participation of fetal factors in maintaining the immune balance during gestation was investigated by assessing the effects of human chorionic gonadotropin (hCG) on murine Treg cells and Th17 cells.

2022-10-14 | PXD035883 | Pride

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data