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Signals triggered by a bacterial pore-forming toxin contribute to toll-like receptor redundancy in gram-positive bacterial recognition.
Molecular Immunology, Helmholtz Centre for Infection Research, Braunschweig, Germany.
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2009 (English)In: Journal of Infectious Diseases, ISSN 0022-1899, E-ISSN 1537-6613, Vol. 199, no 1, 124-33 p.Article in journal (Refereed) Published
Abstract [en]

The results illustrate that signals triggered by LLO contribute to TLR2 redundancy in recognition of L. monocytogenes. Under normal conditions, multiple and, sometimes, redundant pathways cooperate to induce a rapid antimicrobial defense. When one signaling pathway-in this case, TLR2-is removed from the system, the other pathways are still capable of mounting a sufficient response to ensure survival of the host.

Place, publisher, year, edition, pages
2009. Vol. 199, no 1, 124-33 p.
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URN: urn:nbn:se:umu:diva-46332DOI: 10.1086/595562PubMedID: 19032107OAI: oai:DiVA.org:umu-46332DiVA: diva2:437890
Available from: 2011-08-30 Created: 2011-08-30 Last updated: 2017-12-08

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Gekara, Nelson O
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CiteExportLink to record
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