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Schmitz, F.* ; Heit, A.* ; Guggemoos, S. ; Krug, A.* ; Mages, J.* ; Schiemann, M.* ; Adler, H. ; Drexler, I. ; Haas, T.* ; Lang, R.* ; Wagner, H.*

Interferon-regulatory-factor 1 controls Toll-like receptor 9-mediated IFN- production in myeloid dendritic cells.

Eur. J. Immunol. 37, 315-327 (2007)
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Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
Activation of interferon regulatory factor (IRF)-3 and/or IRF-7 drives the expression of antiviral genes and the production of / IFN, a hallmark of antiviral responses triggered by Toll-like receptors (TLR). Here we describe a novel antiviral signaling pathway operating in myeloid (m) dendritic cells (DC) and macrophages that does not require IRF-3 and/or IRF-7 but is driven by IRF-1. IRF-1 together with myeloid differentiation factor 88 (MyD88) or IL-1 receptor-associated kinase (IRAK)-1 triggered IFN- promoter activation. IRF-1 physically interacted with MyD88 and activation of mDC via TLR-9 induced IRF-1-dependent IFN- production paralleled by rapid transcriptional activation of IFN-stimulated genes. The NF-B-dependent production of pro-inflammatory cytokines, however, was not influenced by IRF-1. TLR-9 signaling through this pathway conferred cellular antiviral resistance while IRF-1-deficient mice displayed enhanced susceptibility to viral infection. These results demonstrate that TLR-9 activation of mDC and macrophages contributes to antiviral immunity via IRF-1.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Dendritic cell; Interferon; Interferon regulatory factor-1; Toll-like receptor; xxx
ISSN (print) / ISBN 0014-2980
e-ISSN 1521-4141
Quellenangaben Band: 37, Heft: 2, Seiten: 315-327 Artikelnummer: , Supplement: ,
Verlag Wiley
Verlagsort Hoboken
Begutachtungsstatus Peer reviewed
Institut(e) CCG Hematopoetic Cell Transplants (IMI-KHZ)
Institute of Virology (VIRO)