title: Pattern recognition receptors TLR4 and CD14 mediate response to respiratory syncytial virus.
abstract: The innate immune system contributes to the earliest phase of the host defense against foreign organisms and has both soluble and cellular pattern recognition receptors for microbial products. Two important members of this receptor group, CD14 and the Toll-like receptor (TLR) pattern recognition receptors, are essential for the innate immune response to components of Gram-negative and Gram-positive bacteria, mycobacteria, spirochetes and yeast. We now find that these receptors function in an antiviral response as well. The innate immune response to the fusion protein of an important respiratory pathogen of humans, respiratory syncytial virus (RSV), was mediated by TLR4 and CD14. RSV persisted longer in the lungs of infected TLR4-deficient mice compared to normal mice. Thus, a common receptor activation pathway can initiate innate immune responses to both bacterial and viral pathogens.
authors.affiliation: Department of Medicine, University of Massachusetts Medical School, Worcester, MA 01605, USA. evelyn.kurt-jones@umassmed.edu
authors.forename: E A
authors.initials: EA
authors.lastname: Kurt-Jones
authors.forename: L
authors.initials: L
authors.lastname: Popova
authors.forename: L
authors.initials: L
authors.lastname: Kwinn
authors.forename: L M
authors.initials: LM
authors.lastname: Haynes
authors.forename: L P
authors.initials: LP
authors.lastname: Jones
authors.forename: R A
authors.initials: RA
authors.lastname: Tripp
authors.forename: E E
authors.initials: EE
authors.lastname: Walsh
authors.forename: M W
authors.initials: MW
authors.lastname: Freeman
authors.forename: D T
authors.initials: DT
authors.lastname: Golenbock
authors.forename: L J
authors.initials: LJ
authors.lastname: Anderson
authors.forename: R W
authors.initials: RW
authors.lastname: Finberg
mesh_terms: D000818:Animals; D000911:Antibodies, Monoclonal / Q000494:pharmacology; D016207:Cytokines / Q000096:biosynthesis; D029721:Drosophila Proteins; D006801:Humans; D066298:In Vitro Techniques; D018836:Inflammation Mediators / Q000378:metabolism; D007963:Leukocytes, Mononuclear / Q000276:immunology; D018950:Lipopolysaccharide Receptors / Q000235:genetics / Q000276:immunology*; D008168:Lung / Q000276:immunology / Q000821:virology; D008562:Membrane Glycoproteins / Q000172:deficiency / Q000235:genetics / Q000276:immunology*; D051379:Mice; D018345:Mice, Knockout; D011956:Receptors, Cell Surface / Q000172:deficiency / Q000235:genetics / Q000276:immunology*; D018357:Respiratory Syncytial Virus Infections / Q000276:immunology / Q000821:virology; D012136:Respiratory Syncytial Viruses / Q000276:immunology* / Q000472:pathogenicity*; D051197:Toll-Like Receptor 4; D051193:Toll-Like Receptors; D014760:Viral Fusion Proteins / Q000276:immunology
chemical_list: D000911:Antibodies, Monoclonal; D016207:Cytokines; D029721:Drosophila Proteins; D018836:Inflammation Mediators; D018950:Lipopolysaccharide Receptors; D008562:Membrane Glycoproteins; D011956:Receptors, Cell Surface; C495345:TLR4 protein, human; D051197:Toll-Like Receptor 4; D051193:Toll-Like Receptors; D014760:Viral Fusion Proteins