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      Interfer’n with antibody responses

      Author(s): 1 , 1
      Publication date Created:
      Publication date (Print):
      Journal: Science Immunology
      Publisher: American Association for the Advancement of Science (AAAS)

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          Abstract

          Type I interferon blocks the generation of neutralizing antibodies in response to chronic infection. See related Research Articles by Fallet et al. , Moseman et al. , and Sammicheli et al.

          Abstract

          Type I interferon blocks the generation of neutralizing antibodies in response to chronic infection.

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          Most cited references8

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          Priming of natural killer cells by nonmucosal mononuclear phagocytes requires instructive signals from commensal microbiota.

          Stephanie C. Ganal, Stephanie L. Sanos, Carsten Kallfass … (2012)
          Mononuclear phagocytes are an important component of an innate immune system perceived as a system ready to react upon encounter of pathogens. Here, we show that in response to microbial stimulation, mononuclear phagocytes residing in nonmucosal lymphoid organs of germ-free mice failed to induce expression of a set of inflammatory response genes, including those encoding the various type I interferons (IFN-I). Consequently, NK cell priming and antiviral immunity were severely compromised. Whereas pattern recognition receptor signaling and nuclear translocation of the transcription factors NF-κB and IRF3 were normal in mononuclear phagocytes of germ-free mice, binding to their respective cytokine promoters was impaired, which correlated with the absence of activating histone marks. Our data reveal a previously unrecognized role for postnatally colonizing microbiota in the introduction of chromatin level changes in the mononuclear phagocyte system, thereby poising expression of central inflammatory genes to initiate a powerful systemic immune response during viral infection. Copyright © 2012 Elsevier Inc. All rights reserved.
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            Regulation of antiviral T cell responses by type I interferons.

            Josh Crouse, Ulrich Kalinke, Annette Oxenius (2015)
            Type I interferons (IFNs) are pro-inflammatory cytokines that are rapidly induced in different cell types during viral infections. The consequences of type I IFN signalling include direct antiviral activity, innate immune cell activation and regulation of adaptive immune responses. In this Review, we discuss recent conceptual advances in our understanding of indirect and direct regulation of T cell immunity by type I IFNs, which can either promote or inhibit T cell activation, proliferation, differentiation and survival. This regulation depends, to a large extent, on the timing of type I IFN exposure relative to T cell receptor signalling. Type I IFNs also provide activated T cells with resistance to natural killer cell-mediated elimination.
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              Antiviral antibody responses: the two extremes of a wide spectrum.

              Hans Hengartner, Lars Hangartner, R M Zinkernagel (2006)
              Viruses elicit a diverse spectrum of antiviral antibody responses. In this review, we discuss two widely used experimental model systems for viral infections - non-cytopathic lymphocytic choriomeningitis virus (LCMV) and acutely cytopathic vesicular stomatitis virus (VSV) - to analyse two fundamentally different types of antiviral antibody response. The basic principles found in these model infections are discussed in the context of other viral infections, and with regard to protective neutralizing versus non-protective enzyme-linked immunosorbent assay (ELISA)-detected antibody responses. Issues of antibody specificity, affinity and avidity, maturation and escape are discussed in the context of co-evolution of the host and viruses.
              Article 0 comments Cited 114 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Title: Science Immunology
                Abbreviated Title: Sci. Immunol.
                Publisher: American Association for the Advancement of Science (AAAS)
                ISSN (Electronic): 2470-9468
                Publication date Created: October 21 2016
                Publication date (Print): October 21 2016
                Volume: 1
                Issue: 4
                Affiliations
                [1 ]Department of Microbiology and Immunology and Howard Hughes Medical Institute, University of California San Francisco, San Francisco, CA 94143, USA.
                Article
                DOI: 10.1126/sciimmunol.aaj1836
                PubMed ID: 28783688
                SO-VID: a411a7b5-0f0e-44bc-ad1b-45f6a4b4d461
                Copyright © © 2016
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