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Signals triggered by a bacterial pore-forming toxin contribute to toll-like receptor redundancy in gram-positive bacterial recognition.

Gekara, Nelson O (author)
Molecular Immunology, Helmholtz Centre for Infection Research, Braunschweig, Germany
Dietrich, Nicole (author)
Lyszkiewicz, Marcin (author)
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Lienenklaus, Stefan (author)
Weiss, Siegfried (author)
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 (creator_code:org_t)
2009-01-01
2009
English.
In: Journal of Infectious Diseases. - : Oxford University Press (OUP). - 0022-1899 .- 1537-6613. ; 199:1, s. 124-33
  • Journal article (peer-reviewed)
Abstract Subject headings
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  • 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.

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