Role of Leptin and SOCS3 in Inhibiting the Type I Interferon Response During Obesity.

Abstract:

:Obesity provokes an imbalance in the immune system, including an aberrant type I interferon response during some viral infections and after TLR stimulation. SOCS3 overexpression and altered systemic leptin levels could be responsible for the reduced type I interferon production in people with obesity and, eventually, significantly increase the risk of viral infection. The aim of this study was to determine whether SOCS3- and leptin-induced tolerance are responsible for the reduced type I interferon production in people with obesity. SOCS3 overexpression in PBMCs from people with obesity was inhibited with the small interfering RNA (siRNA) assay, and leptin-induced tolerance was evaluated in PBMCs from non-obese volunte\ers and U937 cells treated with TLR ligands. SOCS3, but not SOCS1, gene silencing via siRNA increased the type I interferon response in PBMCs obtained from people with obesity. On the other hand, leptin induced SOCS3 expression and inhibited type I interferons in PBMCs from healthy donors and in U937 monocytes stimulated with TLR ligands. Taken together, these results demonstrate that reduced type I interferon production in obesity is caused by SOCS3 overexpression as well as tolerance induced by leptin. Here, we demonstrate a key role of leptin and SOCS3 in inhibiting the type I interferon response during obesity.

journal_name

Inflammation

journal_title

Inflammation

authors

Terán-Cabanillas E,Hernández J

doi

10.1007/s10753-016-0452-x

subject

Has Abstract

pub_date

2017-02-01 00:00:00

pages

58-67

issue

1

eissn

0360-3997

issn

1573-2576

pii

10.1007/s10753-016-0452-x

journal_volume

40

pub_type

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