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Curr Opin Immunol. 2017 Jun;46:121-126. doi: 10.1016/j.coi.2017.03.012. Epub 2017 Jun 29.

Reviewing the impact of lipid synthetic flux on Th17 function.

Author information

1
Department of Microbiology, Immunology and Molecular Genetics, David Geffen School of Medicine, University of California, 615 Charles E. Young Drive, Los Angeles, CA 90095, United States.
2
Department of Microbiology, Immunology and Molecular Genetics, David Geffen School of Medicine, University of California, 615 Charles E. Young Drive, Los Angeles, CA 90095, United States; Department of Molecular and Medical Pharmacology, David Geffen School of Medicine, University of California, 615 Charles E. Young Drive, CA 90095, United States. Electronic address: sbensinger@mednet.ucla.edu.

Abstract

CD4+ T helper 17 cells (Th17) acquire specific effector functions in response to activation and instructional signals. Accumulating evidence indicates that specific cellular lipid metabolic pathways play essential roles in regulating the differentiation and function of Th17 cells. Mechanistic studies reveal that metabolic fluxes through both the cholesterol and long chain fatty acid biosynthetic pathways are important in controlling RORγ transcriptional activity through their ability to generate lipid ligands of RORγ. Genetic and pharmacologic studies demonstrate that altering the flux through these lipid biosynthetic pathways impacts the generation of IL-17 as well as the balance of Th17 and CD4+ regulatory T cells (Tregs). In this mini-review, we briefly introduce the mechanics of cholesterol and long chain fatty acid biosynthesis. We also discuss the evidence underlying the unique role that these lipid metabolic pathways play in intrinsically regulating the fate and function of Th17 cells under normal and pathogenic conditions.

PMID:
28668661
DOI:
10.1016/j.coi.2017.03.012
[Indexed for MEDLINE]

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