Document Detail


Type I Interferons Link Viral Infection to Enhanced Epithelial Turnover and Repair.
MedLine Citation:
PMID:  25482432     Owner:  NLM     Status:  Publisher    
Abstract/OtherAbstract:
The host immune system functions constantly to maintain chronic commensal and pathogenic organisms in check. The consequences of these immune responses on host physiology are as yet unexplored, and may have long-term implications in health and disease. We show that chronic viral infection increases epithelial turnover in multiple tissues, and the antiviral cytokines type I interferons (IFNs) mediate this response. Using a murine model with persistently elevated type I IFNs in the absence of exogenous viral infection, the Irgm1(-/-) mouse, we demonstrate that type I IFNs act through nonepithelial cells, including macrophages, to promote increased epithelial turnover and wound repair. Downstream of type I IFN signaling, the highly related IFN-stimulated genes Apolipoprotein L9a and b activate epithelial proliferation through ERK activation. Our findings demonstrate that the host immune response to chronic viral infection has systemic effects on epithelial turnover through a myeloid-epithelial circuit.
Authors:
Lulu Sun; Hiroyuki Miyoshi; Sofia Origanti; Timothy J Nice; Alexandra C Barger; Nicholas A Manieri; Leslie A Fogel; Anthony R French; David Piwnica-Worms; Helen Piwnica-Worms; Herbert W Virgin; Deborah J Lenschow; Thaddeus S Stappenbeck
Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2014-12-3
Journal Detail:
Title:  Cell host & microbe     Volume:  -     ISSN:  1934-6069     ISO Abbreviation:  Cell Host Microbe     Publication Date:  2014 Dec 
Date Detail:
Created Date:  2014-12-8     Completed Date:  -     Revised Date:  2014-12-9    
Medline Journal Info:
Nlm Unique ID:  101302316     Medline TA:  Cell Host Microbe     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Copyright Information:
Copyright © 2015 Elsevier Inc. All rights reserved.
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