Document Detail


The role of IL-10 in regulating immunity to persistent viral infections.
MedLine Citation:
PMID:  20703965     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The immune system has evolved multipronged responses that are critical to effectively defend the body from invading pathogens and to clear infection. However, the same weapons employed to eradicate infection can have caustic effects on normal bystander cells. Therefore, tight regulation is vital and the host must balance engendering correct and sufficient immune responses to pathogens while limiting errant and excessive immunopathology. To accomplish this task, a complex network of positive and negative immune signals are delivered, which in most instances successfully eliminate the pathogen. However, in response to some viral infections, immune function is rapidly suppressed leading to viral persistence. Immune suppression is a critical obstacle to the control of many persistent viral infections such as HIV, hepatitis C, and hepatitis B virus, which together affect more than 500 million individuals worldwide. Thus, the ability to therapeutically enhance immunity is a potentially powerful approach to resolve persistent infections. The host-derived cytokine IL-10 is a key player in the establishment and perpetuation of viral persistence. This chapter discusses the role of IL-10 in viral persistence and explores the exciting prospect of therapeutically blocking IL-10 to increase antiviral immunity and vaccine efficacy.
Authors:
Elizabeth B Wilson; David G Brooks
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review    
Journal Detail:
Title:  Current topics in microbiology and immunology     Volume:  350     ISSN:  0070-217X     ISO Abbreviation:  Curr. Top. Microbiol. Immunol.     Publication Date:  2011  
Date Detail:
Created Date:  2011-04-11     Completed Date:  2011-07-22     Revised Date:  2011-09-21    
Medline Journal Info:
Nlm Unique ID:  0110513     Medline TA:  Curr Top Microbiol Immunol     Country:  Germany    
Other Details:
Languages:  eng     Pagination:  39-65     Citation Subset:  IM    
Affiliation:
Department of Microbiology, Immunology and Molecular Genetics and the UCLA AIDS Institute, David Geffen School of Medicine, University of California, Los Angeles, CA, 90095, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Chronic Disease
Gene Expression Regulation*
Humans
Immunosuppression
Interleukin-10 / genetics,  immunology,  metabolism*
Lymphocyte Activation / drug effects*
Mice
Mice, Knockout
T-Lymphocytes / cytology,  immunology*,  virology
Virus Diseases / immunology*,  virology
Viruses / immunology,  pathogenicity*
Grant Support
ID/Acronym/Agency:
AI082975/AI/NIAID NIH HHS; AI085043/AI/NIAID NIH HHS; R01 AI085043-03/AI/NIAID NIH HHS
Chemical
Reg. No./Substance:
130068-27-8/Interleukin-10

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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