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dc.contributor.authorLoof, Torsten G
dc.contributor.authorGoldmann, Oliver
dc.contributor.authorMedina, Eva
dc.date.accessioned2009-02-02T08:57:16Zen
dc.date.available2009-02-02T08:57:16Zen
dc.date.issued2008-06en
dc.identifier.citationImmune recognition of Streptococcus pyogenes by dendritic cells. 2008, 76 (6):2785-92 Infect. Immun.en
dc.identifier.issn1098-5522en
dc.identifier.pmid18391010en
dc.identifier.doi10.1128/IAI.01680-07en
dc.identifier.urihttp://hdl.handle.net/10033/48314en
dc.description.abstractStreptococcus pyogenes is one of the most frequent human pathogens. Recent studies have identified dendritic cells (DCs) as important contributors to host defense against S. pyogenes. The objective of this study was to identify the receptors involved in immune recognition of S. pyogenes by DCs. To determine whether Toll-like receptors (TLRs) were involved in DC sensing of S. pyogenes, we evaluated the response of bone marrow-derived DCs obtained from mice deficient in MyD88, an adapter molecule used by almost all TLRs, following S. pyogenes stimulation. Despite the fact that MyD88(-/-) DCs did not differ from wild-type DCs in the ability to internalize and kill S. pyogenes, the up-regulation of maturation markers, such as CD40, CD80, and CD86, and the production of inflammatory cytokines, such as interleukin-12 (IL-12), IL-6, and tumor necrosis factor alpha, were dramatically impaired in S. pyogenes-stimulated MyD88(-/-) DCs. These results suggest that signaling through TLRs is the principal pathway by which DCs sense S. pyogenes and become activated. Surprisingly, DCs deficient in signaling through each of the TLRs reported as potential receptors for gram-positive cell components, such as TLR1, TLR2, TLR4, TLR9, and TLR2/6, were not impaired in the secretion of proinflammatory cytokines and the up-regulation of costimulatory molecules after S. pyogenes stimulation. In conclusion, our results exclude a major involvement of a single TLR or the heterodimer TLR2/6 in S. pyogenes sensing by DCs and argue for a multimodal recognition in which a combination of several different TLR-mediated signals is essential for a rapid and effective response to the pathogen.
dc.language.isoenen
dc.subject.meshAnimalsen
dc.subject.meshCells, Cultureden
dc.subject.meshCytokinesen
dc.subject.meshDendritic Cellsen
dc.subject.meshGene Expression Regulationen
dc.subject.meshMiceen
dc.subject.meshMice, Inbred C57BLen
dc.subject.meshMice, Knockouten
dc.subject.meshMyeloid Differentiation Factor 88en
dc.subject.meshPhagocytosisen
dc.subject.meshSpecific Pathogen-Free Organismsen
dc.subject.meshStreptococcus pyogenesen
dc.subject.meshToll-Like Receptor 2en
dc.subject.meshToll-Like Receptor 9en
dc.titleImmune recognition of Streptococcus pyogenes by dendritic cells.en
dc.typeArticleen
dc.contributor.departmentInfection Immunology Research Group, Department of Microbial Pathogenesis, Helmholtz Center for Infection Research, Inhoffenstrasse 7, 38124 Braunschweig, Germany.en
dc.identifier.journalInfection and immunityen
refterms.dateFOA2018-06-13T16:58:11Z
html.description.abstractStreptococcus pyogenes is one of the most frequent human pathogens. Recent studies have identified dendritic cells (DCs) as important contributors to host defense against S. pyogenes. The objective of this study was to identify the receptors involved in immune recognition of S. pyogenes by DCs. To determine whether Toll-like receptors (TLRs) were involved in DC sensing of S. pyogenes, we evaluated the response of bone marrow-derived DCs obtained from mice deficient in MyD88, an adapter molecule used by almost all TLRs, following S. pyogenes stimulation. Despite the fact that MyD88(-/-) DCs did not differ from wild-type DCs in the ability to internalize and kill S. pyogenes, the up-regulation of maturation markers, such as CD40, CD80, and CD86, and the production of inflammatory cytokines, such as interleukin-12 (IL-12), IL-6, and tumor necrosis factor alpha, were dramatically impaired in S. pyogenes-stimulated MyD88(-/-) DCs. These results suggest that signaling through TLRs is the principal pathway by which DCs sense S. pyogenes and become activated. Surprisingly, DCs deficient in signaling through each of the TLRs reported as potential receptors for gram-positive cell components, such as TLR1, TLR2, TLR4, TLR9, and TLR2/6, were not impaired in the secretion of proinflammatory cytokines and the up-regulation of costimulatory molecules after S. pyogenes stimulation. In conclusion, our results exclude a major involvement of a single TLR or the heterodimer TLR2/6 in S. pyogenes sensing by DCs and argue for a multimodal recognition in which a combination of several different TLR-mediated signals is essential for a rapid and effective response to the pathogen.


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