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Cofactors required for TLR7- and TLR9-dependent innate immune responses.

Abstract：

:Pathogens commonly utilize endocytic pathways to gain cellular access. The endosomal pattern recognition receptors TLR7 and TLR9 detect pathogen-encoded nucleic acids to initiate MyD88-dependent proinflammatory responses to microbial infection. Using genome-wide RNAi screening and integrative systems-based analysis, we identify 190 cofactors required for TLR7- and TLR9-directed signaling responses. A set of cofactors were crossprofiled for their activities downstream of several immunoreceptors and then functionally mapped based on the known architecture of NF-κB signaling pathways. Protein complexes and pathways involved in ubiquitin-protein ligase activities, sphingolipid metabolism, chromatin modifications, and ancient stress responses were found to modulate innate recognition of endosomal nucleic acids. Additionally, hepatocyte growth factor-regulated tyrosine kinase substrate (HRS) was characterized as necessary for ubiquitin-dependent TLR9 targeting to the endolysosome. Proteins and pathways identified here should prove useful in delineating strategies to manipulate innate responses for treatment of autoimmune disorders and microbial infection.

journal_name

Cell Host Microbe

journal_title

Cell host & microbe

authors

Chiang CY,Engel A,Opaluch AM,Ramos I,Maestre AM,Secundino I,De Jesus PD,Nguyen QT,Welch G,Bonamy GM,Miraglia LJ,Orth AP,Nizet V,Fernandez-Sesma A,Zhou Y,Barton GM,Chanda SK

doi

10.1016/j.chom.2012.02.002

subject

Has Abstract

pub_date

2012-03-15 00:00:00

pages

306-18

issue

3

eissn

1931-3128

issn

1934-6069

pii

S1931-3128(12)00062-5

journal_volume

11

pub_type

杂志文章

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