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Rab4b Deficiency in T Cells Promotes Adipose Treg/Th17 Imbalance, Adipose Tissue Dysfunction, and Insulin Resistance.

Abstract：

:Obesity modifies T cell populations in adipose tissue, thereby contributing to adipose tissue inflammation and insulin resistance. Here, we show that Rab4b, a small GTPase governing endocytic trafficking, is pivotal in T cells for the development of these pathological events. Rab4b expression is decreased in adipose T cells from mice and patients with obesity. The specific depletion of Rab4b in T cells causes adipocyte hypertrophy and insulin resistance in chow-fed mice and worsens insulin resistance in obese mice. This phenotype is driven by an increase in adipose Th17 and a decrease in adipose Treg due to a cell-autonomous skew of differentiation toward Th17. The Th17/Treg imbalance initiates adipose tissue inflammation and reduces adipogenesis, leading to lipid deposition in liver and muscles. Therefore, we propose that the obesity-induced loss of Rab4b in adipose T cells may contribute to maladaptive white adipose tissue remodeling and insulin resistance by altering adipose T cell fate.

journal_name

Cell Rep

journal_title

Cell reports

authors

Gilleron J,Bouget G,Ivanov S,Meziat C,Ceppo F,Vergoni B,Djedaini M,Soprani A,Dumas K,Jacquel A,Yvan-Charvet L,Venteclef N,Tanti JF,Cormont M

doi

10.1016/j.celrep.2018.11.083

subject

Has Abstract

pub_date

2018-12-18 00:00:00

pages

3329-3341.e5

issue

12

issn

2211-1247

pii

S2211-1247(18)31874-6

journal_volume

25

pub_type

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