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Noncanonical autophagy is required for type I interferon secretion in response to DNA-immune complexes.

Abstract：

:Toll-like receptor-9 (TLR9) is largely responsible for discriminating self from pathogenic DNA. However, association of host DNA with autoantibodies activates TLR9, inducing the pathogenic secretion of type I interferons (IFNs) from plasmacytoid dendritic cells (pDCs). Here, we found that in response to DNA-containing immune complexes (DNA-IC), but not to soluble ligands, IFN-α production depended upon the convergence of the phagocytic and autophagic pathways, a process called microtubule-associated protein 1A/1B-light chain 3 (LC3)-associated phagocytosis (LAP). LAP was required for TLR9 trafficking into a specialized interferon signaling compartment by a mechanism that involved autophagy-related proteins, but not the conventional autophagic preinitiation complex, or adaptor protein-3 (AP-3). Our findings unveil a new role for nonconventional autophagy in inflammation and provide one mechanism by which anti-DNA autoantibodies, such as those found in several autoimmune disorders, bypass the controls that normally restrict the apportionment of pathogenic DNA and TLR9 to the interferon signaling compartment.

journal_name

Immunity

journal_title

Immunity

authors

Henault J,Martinez J,Riggs JM,Tian J,Mehta P,Clarke L,Sasai M,Latz E,Brinkmann MM,Iwasaki A,Coyle AJ,Kolbeck R,Green DR,Sanjuan MA

doi

10.1016/j.immuni.2012.09.014

subject

Has Abstract

pub_date

2012-12-14 00:00:00

pages

986-997

issue

6

eissn

1074-7613

issn

1097-4180

journal_volume

37

pub_type

杂志文章

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