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      Tumor necrosis factor and interferon: cytokines in harmony

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      Author(s): 1 , 1 ,
      Publication date (Electronic):
      Journal: Current Opinion in Microbiology
      Publisher: Elsevier Ltd.

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          Abstract

          Individually, tumor necrosis factor (TNF) and the various interferons frequently display strong antiviral activities. Certain combinations of these cytokines, however, induce a synergistic antiviral state which is distinct from that induced by either one alone. This novel synergistic antiviral state likely occurs through several possible mechanisms, involves multiple signaling pathways, and inhibits a wider range of viruses than the individual cytokines alone. While underappreciated when first discovered, this synergistic phenomenon is proving to be of a much broader scope than initially thought. More work is needed to refine our understanding of this observation and its physiological implications for anti-pathogen responses.

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          Identification of genes differentially regulated by interferon alpha, beta, or gamma using oligonucleotide arrays.

          S. Der, A. Zhou, B R Williams … (1998)
          The pleiotropic activities of interferons (IFNs) are mediated primarily through the transcriptional regulation of many downstream effector genes. The mRNA profiles from IFN-alpha, -beta, or -gamma treatments of the human fibrosarcoma cell line, HT1080, were determined by using oligonucleotide arrays with probe sets corresponding to more than 6,800 human genes. Among these were transcripts for known IFN-stimulated genes (ISGs), the expression of which were consistent with previous studies in which the particular ISG was characterized as responsive to either Type I (alpha, beta) or Type II (gamma) IFNs, or both. Importantly, many novel IFN-stimulated genes were identified that were diverse in their known biological functions. For instance, several novel ISGs were identified that are implicated in apoptosis (including RAP46/Bag-1, phospholipid scramblase, and hypoxia inducible factor-1alpha). Furthermore, several IFN-repressed genes also were identified. These results demonstrate the usefulness of oligonucleotide arrays in monitoring mammalian gene expression on a broad and unprecedented scale. In particular, these findings provide insights into the basic mechanisms of IFN actions and ultimately may contribute to better therapeutic uses for IFNs.
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            Noncytolytic control of viral infections by the innate and adaptive immune response.

            L Guidotti, F V Chisari (2001)
            This review describes the contribution of noncytolytic mechanisms to the control of viral infections with a particular emphasis on the role of cytokines in these processes. It has long been known that most cell types in the body respond to an incoming viral infection by rapidly secreting antiviral cytokines such as interferon alpha/beta (IFN-alpha/beta). After binding to specific receptors on the surface of infected cells, IFN-alpha/beta has the potential to trigger the activation of multiple noncytolytic intracellular antiviral pathways that can target many steps in the viral life cycle, thereby limiting the amplification and spread of the virus and attenuating the infection. Clearance of established viral infections, however, requires additional functions of the immune response. The accepted dogma is that complete clearance of intracellular viruses by the immune response depends on the destruction of infected cells by the effector cells of the innate and adaptive immune system [natural killer (NK) cells and cytotoxic T cells (CTLs)]. This notion, however, has been recently challenged by experimental evidence showing that much of the antiviral potential of these cells reflects their ability to produce antiviral cytokines such as IFN-gamma and tumor necrosis factor (TNF)-alpha at the site of the infection. Indeed, these cytokines can purge viruses from infected cells noncytopathically as long as the cell is able to activate antiviral mechanisms and the virus is sensitive to them. Importantly, the same cytokines also control viral infections indirectly, by modulating the induction, amplification, recruitment, and effector functions of the immune response and by upregulating antigen processing and display of viral epitopes at the surface of infected cells. In keeping with these concepts, it is not surprising that a number of viruses encode proteins that have the potential to inhibit the antiviral activity of cytokines.
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              TNF activates an IRF1-dependent autocrine loop leading to sustained expression of chemokines and STAT1-dependent type I interferon-response genes.

              Xiaoyu Hu, Taras Antoniv, Ji Min … (2008)
              Rapid induction of inflammatory genes by tumor necrosis factor (TNF) has been well studied, but little is known about delayed and chronic TNF responses. Here we investigated the kinetics of primary macrophage responses to TNF and discovered that TNF initiates an interferon-beta-mediated autocrine loop that sustains expression of inflammatory genes and induces delayed expression of interferon-response genes such as those encoding the transcription factors STAT1 and IRF7, which enhance macrophage responses to stimulation of cytokines and Toll-like receptors. TNF-induced interferon-beta production depended on interferon-response factor 1, and downstream gene expression was mediated by synergy between small amounts of interferon-beta and canonical TNF-induced signals. Thus, TNF activates a 'feed-forward' loop that sustains inflammation but avoids the potential toxicity associated with the high interferon production induced by stimulation of Toll-like receptors.
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                Author and article information

                Contributors
                Grant McFadden
                Journal
                Journal ID (nlm-ta): Curr Opin Microbiol
                Journal ID (iso-abbrev): Curr. Opin. Microbiol
                Title: Current Opinion in Microbiology
                Publisher: Elsevier Ltd.
                ISSN (Print): 1369-5274
                ISSN (Electronic): 1879-0364
                Publication date PMC-release: 1 July 2008
                Publication date (Print): August 2008
                Publication date (Electronic): 1 July 2008
                Volume: 11
                Issue: 4
                Pages: 378-383
                Affiliations
                Department of Molecular Genetics and Microbiology, College of Medicine, University of Florida, Academic Research Building, Room R4-295, Gainesville, FL 32610, USA
                Author notes
                [1]

                These authors contributed equally to the work.

                Article
                Publisher ID: S1369-5274(08)00072-6
                DOI: 10.1016/j.mib.2008.05.015
                PMC ID: 7108444
                PubMed ID: 18595771
                SO-VID: 715f08b2-0df5-4490-87b3-853688a1ab0f
                Copyright © Copyright © 2008 Elsevier Ltd. All rights reserved.
                License:

                Since January 2020 Elsevier has created a COVID-19 resource centre with free information in English and Mandarin on the novel coronavirus COVID-19. The COVID-19 resource centre is hosted on Elsevier Connect, the company's public news and information website. Elsevier hereby grants permission to make all its COVID-19-related research that is available on the COVID-19 resource centre - including this research content - immediately available in PubMed Central and other publicly funded repositories, such as the WHO COVID database with rights for unrestricted research re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for free by Elsevier for as long as the COVID-19 resource centre remains active.

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                ScienceOpen disciplines: Microbiology & Virology
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                ScienceOpen disciplines: Microbiology & Virology

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