A Mal functional variant is associated with protection against invasive pneumococcal disease, bacteremia, malaria and tuberculosis View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2007-04

AUTHORS

Chiea C Khor, Stephen J Chapman, Fredrik O Vannberg, Aisling Dunne, Caroline Murphy, Edmund Y Ling, Angela J Frodsham, Andrew J Walley, Otto Kyrieleis, Amir Khan, Christophe Aucan, Shelley Segal, Catrin E Moore, Kyle Knox, Sarah J Campbell, Christian Lienhardt, Anthony Scott, Peter Aaby, Oumou Y Sow, Robert T Grignani, Jackson Sillah, Giorgio Sirugo, Nobert Peshu, Thomas N Williams, Kathryn Maitland, Robert J O Davies, Dominic P Kwiatkowski, Nicholas P Day, Djamel Yala, Derrick W Crook, Kevin Marsh, James A Berkley, Luke A J O'Neill, Adrian V S Hill

ABSTRACT

Toll-like receptors (TLRs) and members of their signaling pathway are important in the initiation of the innate immune response to a wide variety of pathogens. The adaptor protein Mal (also known as TIRAP), encoded by TIRAP (MIM 606252), mediates downstream signaling of TLR2 and TLR4 (refs. 4-6). We report a case-control study of 6,106 individuals from the UK, Vietnam and several African countries with invasive pneumococcal disease, bacteremia, malaria and tuberculosis. We genotyped 33 SNPs, including rs8177374, which encodes a leucine substitution at Ser180 of Mal. We found that heterozygous carriage of this variant associated independently with all four infectious diseases in the different study populations. Combining the study groups, we found substantial support for a protective effect of S180L heterozygosity against these infectious diseases (N = 6,106; overall P = 9.6 x 10(-8)). We found that the Mal S180L variant attenuated TLR2 signal transduction. More... »

PAGES

523-528

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/ng1976

DOI

http://dx.doi.org/10.1038/ng1976

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1018014320

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/17322885


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