PPARγ: a transfactor for Th-cell subsets
- 1Department of Immunology, School of Basic Medical Sciences, Peking University Health Science Center
- 2Division of Life Sciences, Faculty of Science, The Chinese University of Hong Kong
Abstract
Peroxisome proliferator-activated receptor γ (PPARγ) is a ligand-activated nuclear transcription factor that governs helper T cell (Th) immunometabolism and functional differentiation by regulating gene transcription, cellular metabolism, and cytokine microenvironment. In Th1 cells, PPARγ primarily regulates interferon-γ (IFN-γ) secretion. Within Th2 cells, it influences GATA-binding protein 3 (GATA3) expression and provides metabolic support for normal cellular functions. In Th17 cells, it inhibits RAR-related orphan receptor γt ( RORγt ) transcription and suppresses inflammatory signals, thereby alleviating Th17-mediated inflammatory responses. In Tregs, PPARγ aids in cell differentiation by activating forkhead box P3 ( Foxp3 ) transcription and inducing metabolic reprogramming. In Th9 cells, PPARγ promotes the secretion of IL-9. Within Tfh cells, the deficiency of PPARγ leads to an increase in B cell leukemia/lymphoma 6 ( Bcl-6 ) expression. Notably, PPARγ agonists and antagonists effectively preserve Th-cell homeostasis by targeting PPARγ-mediated metabolic and signaling pathways. This review summarizes PPARγ as a crucial transcription factor governing Th-cell responses and elucidates its underlying molecular mechanisms. Based on the evidence predominantly derived from animal models, it lays a foundation for translational research of PPARγ-targeted immunotherapy.
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BibTeX
@article{chen2026pparγ,
title = {{PPARγ: a transfactor for Th-cell subsets}},
author = {Sihang Chen and Ming Chu},
journal = {Frontiers in Immunology},
year = {2026},
month = oct,
doi = {10.3389/fimmu.2026.1937624},
url = {https://www.frontiersin.org/articles/10.3389/fimmu.2026.1937624/full},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - PPARγ: a transfactor for Th-cell subsets
AU - Sihang Chen
AU - Ming Chu
PY - 2026
DA - 2026/10/23
JO - Frontiers in Immunology
DO - 10.3389/fimmu.2026.1937624
UR - https://www.frontiersin.org/articles/10.3389/fimmu.2026.1937624/full
AB - Peroxisome proliferator-activated receptor γ (PPARγ) is a ligand-activated nuclear transcription factor that governs helper T cell (Th) immunometabolism and functional differentiation by regulating gene transcription, cellular metabolism, and cytokine microenvironment. In Th1 cells, PPARγ primarily regulates interferon-γ (IFN-γ) secretion. Within Th2 cells, it influences GATA-binding protein 3 (GATA3) expression and provides metabolic support for normal cellular functions. In Th17 cells, it inhibits RAR-related orphan receptor γt ( RORγt ) transcription and suppresses inflammatory signals, thereby alleviating Th17-mediated inflammatory responses. In Tregs, PPARγ aids in cell differentiation by activating forkhead box P3 ( Foxp3 ) transcription and inducing metabolic reprogramming. In Th9 cells, PPARγ promotes the secretion of IL-9. Within Tfh cells, the deficiency of PPARγ leads to an increase in B cell leukemia/lymphoma 6 ( Bcl-6 ) expression. Notably, PPARγ agonists and antagonists effectively preserve Th-cell homeostasis by targeting PPARγ-mediated metabolic and signaling pathways. This review summarizes PPARγ as a crucial transcription factor governing Th-cell responses and elucidates its underlying molecular mechanisms. Based on the evidence predominantly derived from animal models, it lays a foundation for translational research of PPARγ-targeted immunotherapy.
SN - 1664-3224
ER -