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Updated: Jun 5, 2026

In Vitro Differentiation of Mouse Granulocyte-macrophage-colony-stimulating Factor (GM-CSF)-producing T Helper (THGM) Cells
Published on: September 10, 2018
The transcription factor STAT3 is required for T helper 2 cell development
Gretta L Stritesky1, Rajarajeswari Muthukrishnan, Sarita Sehra
1Department of Pediatrics, Herman B Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN 46202, USA.
Signal transducer and activator of transcription 3 (STAT3) cooperates with STAT6 to promote T helper 2 (Th2) cell development. STAT3 is crucial for Th2 cell differentiation and allergic inflammation, integrating multiple STAT signals.
Area of Science:
- Immunology
- Molecular Biology
- Cell Biology
Background:
- Signal transducer and activator of transcription (STAT) proteins regulate T helper cell differentiation.
- STAT6 is essential for T helper 2 (Th2) cell development, while STAT3 promotes Th17 and follicular helper T cell subsets.
Purpose of the Study:
- To investigate the role of STAT3 in Th2 cell development.
- To elucidate the interaction between STAT3 and STAT6 during Th2 cell differentiation.
Main Methods:
- Analysis of STAT3 activation during Th2 cell development.
- Assessment of STAT3's requirement for Th2-associated gene expression.
- Chromatin immunoprecipitation to determine STAT3 binding sites.
- In vivo studies using STAT3-deficient T cells and ovalbumin-induced allergic inflammation models.
Main Results:
- STAT3 is activated during Th2 cell development and is necessary for Th2 cytokine and transcription factor expression.
- STAT3 directly binds to Th2 cell gene loci and is required for STAT6 binding to its targets.
- STAT3 deficiency in T cells abrogates allergic inflammation in vivo.
Conclusions:
- STAT3 collaborates with STAT6 to promote Th2 cell development.
- Differentiating T helper cells integrate signals from multiple STAT proteins during Th2 cell development.
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