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The contribution of toll-like receptors to the pathogenesis of asthma

dc.contributor.authorPhipps, Simon
dc.contributor.authorLam, Chuan En
dc.contributor.authorFoster, Paul S
dc.contributor.authorMatthaei, Klaus
dc.date.accessioned2015-12-08T22:13:33Z
dc.date.issued2007
dc.date.updated2015-12-08T07:44:14Z
dc.description.abstractAsthma is a major disease in the westernized world and its incidence has significantly increased over the past 40 years. Our understanding of the pathogenesis of asthma remains rudimentary, and for this reason, little has been accomplished by way of targeted intervention, either at a population level (to reduce the overall prevalence) or at an individual level (to treat the cause). Instead, the management strategy currently in use relies on broad-spectrum anti-inflammatory agents, generally glucocorticoids and long-acting β2 agonists. The recent discovery of toll-like receptors (TLRs), with their role as the initiators of the innate immune response and inflammation, suggests that modulating these receptors may be beneficial in the treatment of allergic disorders. We review here the cellular distribution of TLR in the lung and their potential contribution to the processes that promote T helper 2 (Th2) immunity and infection-induced exacerbations of allergic lung disease.
dc.identifier.issn0818-9641
dc.identifier.urihttp://hdl.handle.net/1885/29870
dc.publisherBlackwell Publishing Ltd
dc.sourceImmunology and Cell Biology
dc.subjectKeywords: toll like receptor; allergic disease; asthma; cellular distribution; dendritic cell; disease exacerbation; eosinophil; human; immunomodulation; inflammation; innate immunity; mast cell; microbial contamination; nonhuman; respiratory epithelium; review; Th Asthma; Pathogenesis; Toll-like receptors
dc.titleThe contribution of toll-like receptors to the pathogenesis of asthma
dc.typeJournal article
local.bibliographicCitation.issue6
local.bibliographicCitation.lastpage70
local.bibliographicCitation.startpage463
local.contributor.affiliationPhipps, Simon, University of Newcastle
local.contributor.affiliationLam, Chuan En, University of Newcastle
local.contributor.affiliationFoster, Paul S, College of Medicine, Biology and Environment, ANU
local.contributor.affiliationMatthaei, Klaus, College of Medicine, Biology and Environment, ANU
local.contributor.authoruidFoster, Paul S, u8800551
local.contributor.authoruidMatthaei, Klaus, u8200697
local.description.embargo2037-12-31
local.description.notesImported from ARIES
local.identifier.absfor060111 - Signal Transduction
local.identifier.ariespublicationu4020362xPUB69
local.identifier.citationvolume85
local.identifier.doi10.1038/sj.icb.7100104
local.identifier.scopusID2-s2.0-34548448134
local.type.statusPublished Version

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