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Mol. Cells 2012; 33(3): 217-222

Published online February 28, 2012

https://doi.org/10.1007/s10059-012-2297-y

© The Korean Society for Molecular and Cellular Biology

The Nuclear Receptor PPARs as Important Regulators of T-Cell Functions and Autoimmune Diseases

Je-Min Choi1,2,*, and Alfred L.M. Bothwell3,*

1Department of Life Science, Research Institute for Natural Sciences, Hanyang Universtiy, Seoul 133-791, Korea, 2Hanyang Biomedical Research Institute, Hanyang Universtiy, Seoul 133-791, Korea, 3Department of Immunobiology, Yale University School of Medicine, CT 06520, USA

Correspondence to : *Correspondence: jeminchoi@hanyang.ac.kr (JMC); alfred.bothwell@yale.edu (ALMB)

Received: December 29, 2014; Revised: January 22, 2012; Accepted: February 9, 2012

Abstract

Members of the nuclear receptor superfamily function as transcription factors involved in innate and adaptive im-munity as well as lipid metabolism. These highly conser-ved proteins participate in ligand-dependent or -indepen-dent regulatory mechanisms that affect gene expression. Peroxisome proliferator-activated receptors (PPARs), which include PPAR?, PPAR?/?, and PPAR?, are a group of nuclear receptor proteins that play diverse roles in cellular differentiation, development, and metabolism. Each PPAR subfamily is activated by different endogenous and synthetic ligands. Recent studies using specific ligand treatments and cell type-specific PPAR knockout mice have revealed important roles for these proteins in T-cell-related autoimmune diseases. Moreover, PPARs have been shown to regulate T-cell survival, activation, and CD4+ T helper cell differentiation into the Th1, Th2, Th17, and Treg lineages. Here, we review the studies that provide insight into the important regulatory roles of PPARs in T-cell activation, survival, proliferation, differentiation, and autoimmune disease.

Keywords autoimmune disease, nuclear receptor, PPAR, T cell

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Mol. Cells 2012; 33(3): 217-222

Published online March 31, 2012 https://doi.org/10.1007/s10059-012-2297-y

Copyright © The Korean Society for Molecular and Cellular Biology.

The Nuclear Receptor PPARs as Important Regulators of T-Cell Functions and Autoimmune Diseases

Je-Min Choi1,2,*, and Alfred L.M. Bothwell3,*

1Department of Life Science, Research Institute for Natural Sciences, Hanyang Universtiy, Seoul 133-791, Korea, 2Hanyang Biomedical Research Institute, Hanyang Universtiy, Seoul 133-791, Korea, 3Department of Immunobiology, Yale University School of Medicine, CT 06520, USA

Correspondence to:*Correspondence: jeminchoi@hanyang.ac.kr (JMC); alfred.bothwell@yale.edu (ALMB)

Received: December 29, 2014; Revised: January 22, 2012; Accepted: February 9, 2012

Abstract

Members of the nuclear receptor superfamily function as transcription factors involved in innate and adaptive im-munity as well as lipid metabolism. These highly conser-ved proteins participate in ligand-dependent or -indepen-dent regulatory mechanisms that affect gene expression. Peroxisome proliferator-activated receptors (PPARs), which include PPAR?, PPAR?/?, and PPAR?, are a group of nuclear receptor proteins that play diverse roles in cellular differentiation, development, and metabolism. Each PPAR subfamily is activated by different endogenous and synthetic ligands. Recent studies using specific ligand treatments and cell type-specific PPAR knockout mice have revealed important roles for these proteins in T-cell-related autoimmune diseases. Moreover, PPARs have been shown to regulate T-cell survival, activation, and CD4+ T helper cell differentiation into the Th1, Th2, Th17, and Treg lineages. Here, we review the studies that provide insight into the important regulatory roles of PPARs in T-cell activation, survival, proliferation, differentiation, and autoimmune disease.

Keywords: autoimmune disease, nuclear receptor, PPAR, T cell

Mol. Cells
Dec 31, 2023 Vol.46 No.12, pp. 727~777
COVER PICTURE
Lee et al. (pp. 757-763), show that disruption of ANKS1A promotes the entry of intraflagellar transport trains into cilia, increasing protein transport and forming extracellular vesicles (ECVs). This figure illustrates the abundance of ECVs along the cilia of primary ependymal cells derived from ANKS1A KO mice.

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