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      Ubiquitin in the immune system

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          Abstract

          Ubiquitination is a post-translational modification process that has been implicated in the regulation of innate and adaptive immune responses. There is increasing evidence that both ubiquitination and its reversal, deubiquitination, play crucial roles not only during the development of the immune system but also in the orchestration of an immune response by ensuring the proper functioning of the different cell types that constitute the immune system. Here, we provide an overview of the latest discoveries in this field and discuss how they impact our understanding of the ubiquitin system in host defence mechanisms as well as self-tolerance.

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          The danger model: a renewed sense of self.

          Polly Matzinger (2002)
          For over 50 years immunologists have based their thoughts, experiments, and clinical treatments on the idea that the immune system functions by making a distinction between self and nonself. Although this paradigm has often served us well, years of detailed examination have revealed a number of inherent problems. This Viewpoint outlines a model of immunity based on the idea that the immune system is more concerned with entities that do damage than with those that are foreign.
          Article 0 comments Cited 792 times – based on 0 reviews     Review now
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            Recognition of microorganisms and activation of the immune response.

            Ruslan Medzhitov (2007)
            The mammalian immune system has innate and adaptive components, which cooperate to protect the host against microbial infections. The innate immune system consists of functionally distinct 'modules' that evolved to provide different forms of protection against pathogens. It senses pathogens through pattern-recognition receptors, which trigger the activation of antimicrobial defences and stimulate the adaptive immune response. The adaptive immune system, in turn, activates innate effector mechanisms in an antigen-specific manner. The connections between the various immune components are not fully understood, but recent progress brings us closer to an integrated view of the immune system and its function in host defence.
            Article 0 comments Cited 736 times – based on 0 reviews     Review now
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              Induction of TNF receptor I-mediated apoptosis via two sequential signaling complexes.

              Olivier Micheau, Jurg Tschopp (2003)
              Apoptosis induced by TNF-receptor I (TNFR1) is thought to proceed via recruitment of the adaptor FADD and caspase-8 to the receptor complex. TNFR1 signaling is also known to activate the transcription factor NF-kappa B and promote survival. The mechanism by which this decision between cell death and survival is arbitrated is not clear. We report that TNFR1-induced apoptosis involves two sequential signaling complexes. The initial plasma membrane bound complex (complex I) consists of TNFR1, the adaptor TRADD, the kinase RIP1, and TRAF2 and rapidly signals activation of NF-kappa B. In a second step, TRADD and RIP1 associate with FADD and caspase-8, forming a cytoplasmic complex (complex II). When NF-kappa B is activated by complex I, complex II harbors the caspase-8 inhibitor FLIP(L) and the cell survives. Thus, TNFR1-mediated-signal transduction includes a checkpoint, resulting in cell death (via complex II) in instances where the initial signal (via complex I, NF-kappa B) fails to be activated.
              Article 0 comments Cited 697 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): EMBO Rep
                Journal ID (iso-abbrev): EMBO Rep
                Journal ID (publisher-id): embr
                Title: EMBO Reports
                Publisher: BlackWell Publishing Ltd (Oxford, UK )
                ISSN (Print): 1469-221X
                ISSN (Electronic): 1469-3178
                Publication date (Print): January 2014
                Publication date (Electronic): 27 December 2013
                Volume: 15
                Issue: 1
                Pages: 28-45
                Affiliations
                Centre for Cell Death, Cancer, and Inflammation (CCCI), UCL Cancer Institute, University College London London, UK
                Author notes
                * Corresponding author. Tel: +44 207 679 46471; Fax: +44 207 679 6925; E-mail: h.walczak@ 123456ucl.ac.uk

                These authors contributed equally to the review.

                See the Glossary for abbreviations used in this article.

                Article
                DOI: 10.1002/embr.201338025
                PMC ID: 4303447
                PubMed ID: 24375678
                SO-VID: 59396e27-4f99-41f5-82de-2b2ece89a68e
                Copyright © © 2014 The Authors.
                License:

                This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 24 September 2013
                Date revision received : 11 November 2013
                Date accepted : 13 November 2013
                Categories
                Subject: Reviews
                Subject: “Ubiquitylation: mechanism and functions” Review series

                ScienceOpen disciplines: Molecular biology
                Keywords: autoimmunity,dubs,e3 ligases,inflammation,lubac
                Data availability:
                ScienceOpen disciplines: Molecular biology
                Keywords: autoimmunity, dubs, e3 ligases, inflammation, lubac

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