Linked Life Data

17157070

Source:http://linkedlifedata.com/resource/pubmed/id/17157070

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2007-2-13
pubmed:abstractText
Human primary immunodeficiencies affecting Toll-like receptor (TLR) signalling reveal a non-redundant role for TLR function in defense against pneumococcal infection. To determine the clinical relevance of TLR abnormalities, we studied a population predicted to be enriched for TLR defects-healthy children who had developed invasive pneumococcal infection in the absence of classic risk factors for infection. We describe the development and optimization of a peripheral blood TLR assay. By testing 38 healthy control neonates, children and adults we demonstrated that TLR function was stable over the first six decades of life. We tested 50 children with a history of invasive pneumococcal infection and although TLR defects were predicted to be over-represented in this population, we did not identify any TLR abnormalities. Although TLR signalling defects are associated with greatly enhanced susceptibility to invasive pneumococcal infection, our results suggest that routine clinical screening for TLR defects in healthy children who develop invasive pneumococcal infection is not justified.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
1521-6616
pubmed:author
pubmed:issnType
Print
pubmed:volume
122
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
271-8
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:year
2007
pubmed:articleTitle
Prevalence of Toll-like receptor signalling defects in apparently healthy children who developed invasive pneumococcal infection.
pubmed:affiliation
Department of Paediatrics, BC Children's Hospital and Child and Family Research Institute, University of British Columbia, Vancouver, BC, Canada.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't