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In Vitro Differentiation of Mouse Granulocyte-macrophage-colony-stimulating Factor GM-CSF-producing T Helper THGM Cells
Published on: September 10, 2018
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Polyamines polarized Th2/Th9 cell-fate decision by regulating GATA3 expression.
Atsuo Nakamura1, Daisuke Takahashi2, Yutaka Nakamura2
1Division of Biochemistry, Faculty of Pharmacy and Graduate School of Pharmaceutical Science, Keio University, Minato-ku, Tokyo, Japan; Dairy Science and Technology Institute, Kyodo Milk Industry Co Ltd., Hinode-machi, Tokyo, Japan.
Archives of Biochemistry and Biophysics
|September 18, 2020
Summary
Polyamines are crucial for T helper 2 (Th2) cell development. Inhibiting polyamine synthesis promotes Th9 cells, indicating polyamines regulate the Th2/Th9 balance.
Area of Science:
- Immunology
- Cell Biology
- Biochemistry
Background:
- Polyamines are bioactive molecules with known anti-inflammatory effects.
- The role of polyamines in CD4+ T cell differentiation is not well understood.
Purpose of the Study:
- To investigate the impact of polyamines on naïve CD4+ T cell fate decisions.
- To elucidate the role of polyamines in the regulation of T helper 2 (Th2) and T helper 9 (Th9) cell differentiation.
Main Methods:
- In vitro studies using CD4+ T cells treated with DL-2-difluoromethylornithine (DFMO), a polyamine synthesis inhibitor.
- Transcriptome analysis to assess gene expression changes.
- In vivo studies involving oral administration of DFMO in mice.
Main Results:
- Endogenous polyamines are essential for Th2 cell development, evidenced by reduced GATA3 expression upon DFMO treatment.
- DFMO treatment led to upregulation of Th9-related genes (Il9, Irf4, Batf3) even under Th2-skewing conditions.
- Polyamines regulate the balance between Th2 and Th9 cell differentiation, with depletion favoring Th9 development.
Conclusions:
- Polyamines play a critical role in determining CD4+ T cell fate, specifically in balancing Th2 and Th9 responses.
- Targeting polyamine metabolism may offer therapeutic strategies for immune-mediated diseases by modulating T cell differentiation.
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