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Toll-like receptor cross-hyporesponsiveness is functional in interleukin-1-receptor-associated kinase-1 (IRAK-1)-deficient macrophages: differential role played by IRAK-1 in regulation of tumour necrosis factor and interleukin-10 production
Inst. för Biomedicin, göteborgs Universitet.
Department of Pediatrics and Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX, USA .
Örebro universitet, Hälsoakademin.ORCID-id: 0000-0001-5460-8888
Department of Clinical Microbiology, Orebro University Hospital, Orebro, Sweden .
2008 (Engelska)Ingår i: Scandinavian Journal of Immunology, ISSN 0300-9475, E-ISSN 1365-3083, Vol. 67, nr 5, s. 473-479Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

Signalling downstream Toll-like receptors (TLR) is regulated at several levels in order to activate the immune response and prevent excessive inflammation. Altered intracellular signalling may be one reason that repeated stimulation of various TLRs results in hyporesponsiveness and cross-tolerance. We report that TLR cross-tolerance is inducible in the absence of interleukin-1 receptor-associated kinase-1 (IRAK-1) in peritoneal macrophages. Similar to wild-type macrophages, IRAK-1-deficient macrophages respond with decreased tumour necrosis factor (TNF) production to a secondary TLR stimulation, but in opposite to IRAK-1(+/+), IRAK-1(-/-) macrophages display increased interleukin (IL)-10 production at TLR restimulation. IRAK-1-deficient peritoneal macrophages have a defective TNF and IL-10 production in response to lipoteichoic acid stimulation as well as a defective IL-10-but a normal TNF production in response to high concentration of lipopolysaccharide. Our results demonstrate that IRAK-1 is not necessary for induction of TLR cross-tolerance as judged by TNF production.

Ort, förlag, år, upplaga, sidor
2008. Vol. 67, nr 5, s. 473-479
Nationell ämneskategori
Medicin och hälsovetenskap
Forskningsämne
Immunologi
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URN: urn:nbn:se:oru:diva-6103DOI: 10.1111/j.1365-3083.2008.02096.xPubMedID: 18405325OAI: oai:DiVA.org:oru-6103DiVA, id: diva2:209460
Tillgänglig från: 2009-03-25 Skapad: 2009-03-25 Senast uppdaterad: 2017-12-13Bibliografiskt granskad

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Hultgren-Hörnquist, ElisabethHultgren, Olof H.

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