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Isolation and Th17 Differentiation of Naïve CD4 T Lymphocytes
Published on: September 26, 2013
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The AP-1 transcription factor JunB is required for Th17 cell differentiation
Soh Yamazaki1,2, Yoshihiko Tanaka3,4, Hiromitsu Araki1
1Department of Biochemistry, Kyushu University Graduate School of Medical Sciences, Fukuoka, 812-8582, Japan.
Scientific Reports
|December 14, 2017
Summary
The transcription factor JunB is essential for the development of T helper 17 (Th17) cells, which play key roles in immunity and autoimmune diseases. JunB deficiency prevents Th17 cell differentiation and protects against Th17-mediated inflammation.
Area of Science:
- Immunology
- Molecular Biology
- Cell Biology
Background:
- T helper 17 (Th17) cells are critical for combating extracellular microbes.
- Dysregulated Th17 cell activity contributes to autoimmune diseases.
- Transcription factors regulate T helper cell subset differentiation.
Purpose of the Study:
- To investigate the role of the AP-1 transcription factor JunB in Th17 cell development.
- To elucidate the molecular mechanisms by which JunB controls Th17 cell fate.
Main Methods:
- Genetic deletion of Junb in CD4+ T cells.
- In vitro differentiation assays for various T helper subsets.
- RNA-sequencing (RNA-seq) transcriptome analysis.
- Experimental autoimmune encephalomyelitis (EAE) induction in Junb-deficient mice.
Main Results:
- Junb-deficient CD4+ T cells failed to differentiate into Th17 cells in vitro.
- RNA-seq revealed JunB's critical role in the Th17-specific gene expression program.
- Junb-deficient mice were resistant to EAE, a Th17-mediated disease.
- JunB heterodimerizes with BATF to activate Th17 signature genes, including RORγt and RORα, while suppressing Foxp3.
Conclusions:
- JunB is indispensable for Th17 cell development and function.
- JunB acts through BATF to orchestrate the Th17 lineage specification program.
- Targeting JunB may offer a therapeutic strategy for Th17-mediated autoimmune disorders.
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