A Metabolic Switch for Th17 Pathogenicity

Fred P Davis; Yuka Kanno; John J O'Shea

doi:10.1016/j.cell.2015.11.033

A Metabolic Switch for Th17 Pathogenicity

Cell. 2015 Dec 3;163(6):1308-10. doi: 10.1016/j.cell.2015.11.033.

Authors

Fred P Davis¹, Yuka Kanno², John J O'Shea³

Affiliations

¹ Molecular Immunology and Inflammation Branch, NIAMS, National Institutes of Health, Bethesda, MD 20892, USA. Electronic address: fred.davis@nih.gov.
² Molecular Immunology and Inflammation Branch, NIAMS, National Institutes of Health, Bethesda, MD 20892, USA.
³ Molecular Immunology and Inflammation Branch, NIAMS, National Institutes of Health, Bethesda, MD 20892, USA. Electronic address: john.oshea@nih.gov.

PMID: 26638065
DOI: 10.1016/j.cell.2015.11.033

Abstract

T helper 17 (Th17) cells are critical for host defense but can also drive autoimmunity. This divergent behavior is explored by Gaublomme et al. and Wang et al., who identify inflammation-associated genes by measuring gene expression in nearly 1,000 individual Th17 cells and show that CD5L affects the expression of pro-inflammatory genes by altering lipid synthesis.

Publication types

Comment

MeSH terms

Animals
Encephalomyelitis, Autoimmune, Experimental / pathology*
Humans
Sequence Analysis, RNA*
Single-Cell Analysis*
Th17 Cells / metabolism*
Th17 Cells / pathology*