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Interferon-β Production via Dectin-1-Syk-IRF5 Signaling in Dendritic Cells Is Crucial for Immunity to C.albicans

Abstract:
Type I interferon (IFN) is crucial during infection through its antiviral properties and by coordinating the immunocompetent cells involved in antiviral or antibacterial immunity. Type I IFN (IFN-α and IFN-β) is produced after virus or bacteria recognition by cytosolic receptors or membrane-bound TLR receptors following the activation of the transcription factors IRF3 or IRF7. IFN-β production after fungal infection was recently reported, although the underlying mechanism remains controversial. Here we describe that IFN-β production by dendritic cells (DCs) induced by Candida albicans is largely dependent on Dectin-1- and Dectin-2-mediated signaling. Dectin-1-induced IFN-β production required the tyrosine kinase Syk and the transcription factor IRF5. Type I IFN receptor-deficient mice had a lower survival after C.albicans infection, paralleled by defective renal neutrophil infiltration. IFN-β production by renal infiltrating leukocytes was severely reduced in C.albicans-infected mice with Syk-deficient DCs. These data indicate that Dectin-induced IFN-β production by renal DCs is crucial for defense against C.albicans infection. © 2013 Elsevier Inc.

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Publisher copy:
10.1016/j.immuni.2013.05.010

Authors

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Institution:
University of Oxford
Division:
MSD
Department:
NDORMS
Role:
Author


Journal:
Immunity More from this journal
Volume:
38
Issue:
6
Pages:
1176-1186
Publication date:
2013-06-27
DOI:
EISSN:
1097-4180
ISSN:
1074-7613


Language:
English
Pubs id:
pubs:412078
UUID:
uuid:02c6d9bd-4e4f-444d-9d28-c69bcd71a575
Local pid:
pubs:412078
Source identifiers:
412078
Deposit date:
2013-11-16
ARK identifier:

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