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      Type I interferon: friend or foe?

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      Publication date (Print):
      Journal: The Journal of Experimental Medicine
      Publisher: The Rockefeller University Press

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          Abstract

          Although the role of type I interferon (IFN) in the protection against viral infections has been known and studied for decades, its role in other immunologically relevant scenarios, including bacterial infections, shock, autoimmunity, and cancer, is less well defined and potentially much more complicated.

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          Multiple Sclerosis

          John H Noseworthy, Claudia Lucchinetti, Moses Rodriguez … (2000)
          New England Journal of Medicine, 343(13), 938-952
          Article 0 comments Cited 663 times – based on 0 reviews     Review now
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            Plasmacytoid dendritic cells in immunity.

            Marco Colonna, Giorgio Trinchieri, Yong-Jun Liu (2004)
            Human and mouse plasmacytoid dendritic cells have been shown to correspond to a specialized cell population that produces large amounts of type I interferons in response to viruses, the so-called natural interferon-producing cells. As a result, intensive investigation is now focused on the potential functions of plasmacytoid dendritic cells in both innate and adaptive immunity. Here we review recent progress on the characterization of plasmacytoid dendritic cell origin, development, migration and function in immunity and tolerance, as well as their effect on human diseases.
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              Specificity in Toll-like receptor signalling through distinct effector functions of TRAF3 and TRAF6.

              Hans Häcker, Vanessa Redecke, Blagoy Blagoev … (2006)
              Toll-like receptors (TLRs) are activated by pathogen-associated molecular patterns to induce innate immune responses and production of pro-inflammatory cytokines, interferons and anti-inflammatory cytokines. TLRs activate downstream effectors through adaptors that contain Toll/interleukin-1 receptor (TIR) domains, but the mechanisms accounting for diversification of TLR effector functions are unclear. To dissect biochemically TLR signalling, we established a system for isolating signalling complexes assembled by dimerized adaptors. Using MyD88 as a prototypical adaptor, we identified TNF receptor-associated factor 3 (TRAF3) as a new component of TIR signalling complexes that is recruited along with TRAF6. Using myeloid cells from TRAF3- and TRAF6-deficient mice, we show that TRAF3 is essential for the induction of type I interferons (IFN) and the anti-inflammatory cytokine interleukin-10 (IL-10), but is dispensable for expression of pro-inflammatory cytokines. In fact, TRAF3-deficient cells overproduce pro-inflammatory cytokines owing to defective IL-10 production. Despite their structural similarity, the functions of TRAF3 and TRAF6 are largely distinct. TRAF3 is also recruited to the adaptor TRIF (Toll/IL-1 receptor domain-containing adaptor-inducing IFN-beta) and is required for marshalling the protein kinase TBK1 (also called NAK) into TIR signalling complexes, thereby explaining its unique role in activation of the IFN response.
              Article 0 comments Cited 244 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): J Exp Med
                Journal ID (iso-abbrev): J. Exp. Med
                Journal ID (hwp): jem
                Title: The Journal of Experimental Medicine
                Publisher: The Rockefeller University Press
                ISSN (Print): 0022-1007
                ISSN (Electronic): 1540-9538
                Publication date (Print): 27 September 2010
                Volume: 207
                Issue: 10
                Pages: 2053-2063
                Affiliations
                Cancer and Inflammation Program, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Frederick, MD 21702
                Author notes
                CORRESPONDENCE Giorgio Trinchieri: trinchig@ 123456mail.nih.gov
                Article
                Publisher ID: 20101664
                DOI: 10.1084/jem.20101664
                PMC ID: 2947062
                PubMed ID: 20837696
                SO-VID: 88404eae-d0ba-4805-aac8-b88a02dfb736
                Copyright © Copyright © 2010 by the Rockefeller University Press
                License:

                This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/).

                History
                Date received : 11 August 2010
                Date accepted : 30 August 2010
                Categories
                Subject: Review

                ScienceOpen disciplines: Medicine
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                ScienceOpen disciplines: Medicine

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