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Dead Cells Induce Innate Anergy via Mertk after Acute Viral Infection.

Abstract：

:Infections can result in a temporarily restricted unresponsiveness of the innate immune response, thereby limiting pathogen control. Mechanisms of such unresponsiveness are well studied in lipopolysaccharide tolerance; however, whether mechanisms of tolerance limit innate immunity during virus infection remains unknown. Here, we find that infection with the highly cytopathic vesicular stomatitis virus (VSV) leads to innate anergy for several days. Innate anergy is associated with induction of apoptotic cells, which activates the Tyro3, Axl, and Mertk (TAM) receptor Mertk and induces high levels of interleukin-10 (IL-10) and transforming growth factor β (TGF-β). Lack of Mertk in Mertk-/- mice prevents induction of IL-10 and TGF-β, resulting in abrogation of innate anergy. Innate anergy is associated with enhanced VSV replication and poor survival after infection. Mechanistically, Mertk signaling upregulates suppressor of cytokine signaling 1 (SOCS1) and SOCS3. Dexamethasone treatment upregulates Mertk and enhances innate anergy in a Mertk-dependent manner. In conclusion, we identify Mertk as one major regulator of innate tolerance during infection with VSV.

journal_name

Cell Rep

journal_title

Cell reports

authors

Adomati T,Cham LB,Hamdan TA,Bhat H,Duhan V,Li F,Ali M,Lang E,Huang A,Naser E,Khairnar V,Friedrich SK,Lang J,Friebus-Kardash J,Bergerhausen M,Schiller M,Machlah YM,Lang F,Häussinger D,Ferencik S,Hardt C,Lang PA,

doi

10.1016/j.celrep.2020.02.101

subject

Has Abstract

pub_date

2020-03-17 00:00:00

pages

3671-3681.e5

issue

11

issn

2211-1247

pii

S2211-1247(20)30275-8

journal_volume

30

pub_type

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