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      Complement System Part II: Role in Immunity

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          The complement system has been considered for a long time as a simple lytic cascade, aimed to kill bacteria infecting the host organism. Nowadays, this vision has changed and it is well accepted that complement is a complex innate immune surveillance system, playing a key role in host homeostasis, inflammation, and in the defense against pathogens. This review discusses recent advances in the understanding of the role of complement in physiology and pathology. It starts with a description of complement contribution to the normal physiology (homeostasis) of a healthy organism, including the silent clearance of apoptotic cells and maintenance of cell survival. In pathology, complement can be a friend or a foe. It acts as a friend in the defense against pathogens, by inducing opsonization and a direct killing by C5b–9 membrane attack complex and by triggering inflammatory responses with the anaphylatoxins C3a and C5a. Opsonization plays also a major role in the mounting of an adaptive immune response, involving antigen presenting cells, T-, and B-lymphocytes. Nevertheless, it can be also an enemy, when pathogens hijack complement regulators to protect themselves from the immune system. Inadequate complement activation becomes a disease cause, as in atypical hemolytic uremic syndrome, C3 glomerulopathies, and systemic lupus erythematosus. Age-related macular degeneration and cancer will be described as examples showing that complement contributes to a large variety of conditions, far exceeding the classical examples of diseases associated with complement deficiencies. Finally, we discuss complement as a therapeutic target.

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          Most cited references 238

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          Classification of cell death: recommendations of the Nomenclature Committee on Cell Death 2009.

          Different types of cell death are often defined by morphological criteria, without a clear reference to precise biochemical mechanisms. The Nomenclature Committee on Cell Death (NCCD) proposes unified criteria for the definition of cell death and of its different morphologies, while formulating several caveats against the misuse of words and concepts that slow down progress in the area of cell death research. Authors, reviewers and editors of scientific periodicals are invited to abandon expressions like 'percentage apoptosis' and to replace them with more accurate descriptions of the biochemical and cellular parameters that are actually measured. Moreover, at the present stage, it should be accepted that caspase-independent mechanisms can cooperate with (or substitute for) caspases in the execution of lethal signaling pathways and that 'autophagic cell death' is a type of cell death occurring together with (but not necessarily by) autophagic vacuolization. This study details the 2009 recommendations of the NCCD on the use of cell death-related terminology including 'entosis', 'mitotic catastrophe', 'necrosis', 'necroptosis' and 'pyroptosis'.
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            Atypical hemolytic-uremic syndrome.

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              Complement. Second of two parts.


                Author and article information

                URI : http://frontiersin.org/people/u/211378
                URI : http://frontiersin.org/people/u/238813
                URI : http://frontiersin.org/people/u/203575
                Front Immunol
                Front Immunol
                Front. Immunol.
                Frontiers in Immunology
                Frontiers Media S.A.
                26 May 2015
                : 6
                1UMRS 1138, Centre de Recherche des Cordeliers, INSERM , Paris, France
                2UMRS 1138, Centre de Recherche des Cordeliers, Sorbonne Paris Cité, Université Paris Descartes , Paris, France
                3UMRS 1138, Centre de Recherche des Cordeliers, Sorbonne Universités, UPMC Université Paris 06 , Paris, France
                4Ecole Pratique des Hautes Études (EPHE) , Paris, France
                5Service d’Immunologie Biologique, Assistance Publique-Hôpitaux de Paris, Hôpital Européen Georges-Pompidou , Paris, France
                Author notes

                Edited by: Cordula M. Stover, University of Leicester, UK

                Reviewed by: Robert Braidwood Sim, University of Leicester, UK; Kenneth Reid, University of Oxford, UK

                *Correspondence: Lubka T. Roumenina, Centre de Recherche des Cordeliers, 15 rue de l’Ecole de Médecine, Paris, France, lubka.roumenina@ 123456crc.jussieu.fr

                Specialty section: This article was submitted to Molecular Innate Immunity, a section of the journal Frontiers in Immunology

                Copyright © 2015 Merle, Noe, Halbwachs-Mecarelli, Fremeaux-Bacchi and Roumenina.

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                Page count
                Figures: 12, Tables: 0, Equations: 0, References: 282, Pages: 26, Words: 21023
                Funded by: SIRIC-CARPEM
                Award ID: ARC no. PJA 20141201954
                Funded by: ANR Genopath 2009–2012
                Award ID: 09geno03101I
                Funded by: APHP-PHRC
                Award ID: AOM08198
                Funded by: EU FP7
                Award ID: 2012-305608


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