tetano
Editor, Senior Moderator
J Biomed Biotechnol. 2012;2012:732191. Epub 2012 May 16.
Soluble host defense lectins in innate immunity to influenza virus.
Ng WC, Tate MD, Brooks AG, Reading PC.
Source
Department of Microbiology and Immunology, The University of Melbourne, Parkville, VIC 3010, Australia.
Abstract
Host defenses against viral infections depend on a complex interplay of innate (nonspecific) and adaptive (specific) components. In the early stages of infection, innate mechanisms represent the main line of host defense, acting to limit the spread of virus in host tissues prior to the induction of the adaptive immune response. Serum and lung fluids contain a range of lectins capable of recognizing and destroying influenza A viruses (IAV). Herein, we review the mechanisms by which soluble endogenous lectins mediate anti-IAV activity, including their role in modulating IAV-induced inflammation and disease and their potential as prophylactic and/or therapeutic treatments during severe IAV-induced disease.
PMID:
22665991
[PubMed - in process]
PMCID:
PMC3362216
Free full text
http://www.ncbi.nlm.nih.gov/pubmed/22665991
Soluble host defense lectins in innate immunity to influenza virus.
Ng WC, Tate MD, Brooks AG, Reading PC.
Source
Department of Microbiology and Immunology, The University of Melbourne, Parkville, VIC 3010, Australia.
Abstract
Host defenses against viral infections depend on a complex interplay of innate (nonspecific) and adaptive (specific) components. In the early stages of infection, innate mechanisms represent the main line of host defense, acting to limit the spread of virus in host tissues prior to the induction of the adaptive immune response. Serum and lung fluids contain a range of lectins capable of recognizing and destroying influenza A viruses (IAV). Herein, we review the mechanisms by which soluble endogenous lectins mediate anti-IAV activity, including their role in modulating IAV-induced inflammation and disease and their potential as prophylactic and/or therapeutic treatments during severe IAV-induced disease.
PMID:
22665991
[PubMed - in process]
PMCID:
PMC3362216
Free full text
http://www.ncbi.nlm.nih.gov/pubmed/22665991