Lynch, Lydia and Nowak, Michael and Varghese, Bindu and Clark, Justice and Hogan, Andrew E. and Toxavidis, Vasillis and Balk, Steven P. and O'Shea, Donal and O'Farrelly, Cliona and Exley, Mark A. (2012) Adipose Tissue Invariant NKT Cells Protect against Diet-Induced Obesity and Metabolic Disorder through Regulatory Cytokine Production. Immunity, 37 (3). pp. 574-587. ISSN 1097-4180

Preview

Download (2MB) | Preview

Abstract

Invariant natural killer T (iNKT) cells are evolutionarily conserved innate T cells that influence inflammatory responses. We have shown that iNKT cells, previously thought to be rare in humans, were highly enriched in human and murine adipose tissue, and that as adipose tissue expanded in obesity, iNKT cells were depleted, correlating with proinflammatory macrophage infiltration. iNKT cell numbers were restored in mice and humans after weight loss. Mice lacking iNKT cells had enhanced weight gain, larger adipocytes, fatty livers, and insulin resistance on a high-fat diet. Adoptive transfer of iNKT cells into obese mice or in vivo activation of iNKT cells via their lipid ligand, alpha-galactocylceramide, decreased body fat, triglyceride levels, leptin, and fatty liver and improved insulin sensitivity through anti-inflammatory cytokine production by adiposederived iNKT cells. This finding highlights the potential of iNKT cell-targeted therapies, previously proven to be safe in humans, in the management of obesity and its consequences.

Item Type:	Article
Keywords:	Adipose Tissue; Invariant; NKT Cells; Diet-Induced Obesity; Metabolic Disorder; Regulatory Cytokine Production;
Academic Unit:	Faculty of Science and Engineering > Biology
Item ID:	12431
Identification Number:	https://doi.org/10.1016/j.immuni.2012.06.016
Depositing User:	Andrew Hogan
Date Deposited:	17 Feb 2020 15:54
Journal or Publication Title:	Immunity
Publisher:	Elsevier
Refereed:	Yes
URI:	Publisher
Use Licence:	This item is available under a Creative Commons Attribution Non Commercial Share Alike Licence (CC BY-NC-SA). Details of this licence are available here

Repository Staff Only(login required)

Item control page

Downloads

Origin of downloads