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Notch-RBP-J signaling regulates the transcription factor IRF8 to promote inflammatory macrophage polarization.

Abstract：

:Emerging concepts suggest that the functional phenotype of macrophages is regulated by transcription factors that define alternative activation states. We found that RBP-J, the main nuclear transducer of signaling via Notch receptors, augmented Toll-like receptor 4 (TLR4)-induced expression of key mediators of classically activated M1 macrophages and thus of innate immune responses to Listeria monocytogenes. Notch-RBP-J signaling controlled expression of the transcription factor IRF8 that induced downstream M1 macrophage-associated genes. RBP-J promoted the synthesis of IRF8 protein by selectively augmenting kinase IRAK2-dependent signaling via TLR4 to the kinase MNK1 and downstream translation-initiation control through eIF4E. Our results define a signaling network in which signaling via Notch-RBP-J and TLRs is integrated at the level of synthesis of IRF8 protein and identify a mechanism by which heterologous signaling pathways can regulate the TLR-induced inflammatory polarization of macrophages.

journal_name

Nat Immunol

journal_title

Nature immunology

authors

Xu H,Zhu J,Smith S,Foldi J,Zhao B,Chung AY,Outtz H,Kitajewski J,Shi C,Weber S,Saftig P,Li Y,Ozato K,Blobel CP,Ivashkiv LB,Hu X

doi

10.1038/ni.2304

subject

Has Abstract

pub_date

2012-05-20 00:00:00

pages

642-50

issue

7

eissn

1529-2908

issn

1529-2916

pii

ni.2304

journal_volume

13

pub_type

杂志文章

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