The Inflammasomes
The inflammasome was first described in 2002 as a molecular complex activating proinflammatory caspases and therefore regulating the maturation and biological activities of cytokines such as IL-1 and IL-18. This finding was substantiated by the identific
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Isabelle Couillin Fabio Martinon
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Virginie Pe´trilli
Editors
The Inflammasomes
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Editors Dr. Isabelle Couillin Molecular Immunology and Embryology UMR6218, University of Orleans and CNRS 3B rue de la Fe´rollerie 45071 Orleans France [email protected]
Dr. Virginie Pe´trilli Department Immunity, Microenvironment and Virus Centre de Recherche en Cance´rologie de Lyon 28 rue Laennec 69008 Lyon France [email protected]
Dr. Fabio Martinon Harvard School of Public Health Department of Immunology & Infectious Diseases Huntington Avenue 651 02115-6017 Boston Massachusetts USA [email protected]
Series Editor Prof. Dr. Michael J. Parnham Director of Science MediMlijeko d.o.o. Pozarinje 7 HR-10000 Zagreb Croatia
ISBN 978-3-0348-0147-8 e-ISBN 978-3-0348-0148-5 DOI 10.1007/978-3-0348-0148-5 Library of Congress Control Number: 2011932722 # Springer Basel AG 2011 This work is subject to copyright. All rights are reserved, whether the whole or part of the material is concerned, specifically the rights of translation, reprinting, re-use of illustrations, recitation, broadcasting, reproduction on microfilms or in other ways, and storage in data banks. For any kind of use permission of the copyright owner must be obtained. Cover design: deblik, Berlin Printed on acid-free paper Springer Basel AG is part of Springer Science+Business Media (www.springer.com)
Preface
Innate immunity has been viewed as the first line of defense discriminating “self” (host proteins) from “non-self” (microorganisms). However, emerging literature suggests that innate immunity actually serves as a sophisticated system for sensing signals of “danger” such as pathogenic microbes or host-derived signals of cellular stress, while remaining unresponsive to non-dangerous motifs, such as normal host molecules. The innate immune system engages an array of pattern-recognition receptors (PRRs) to detect invariant microbial motifs. PRRs are expressed by cells at the frontline of defense against infection, including macrophages, monocytes, dendritic cells, neutrophils, and epithelial cells, as well as cells of the adaptive immune system. The discovery of Toll-like receptors (TLRs) provided a class of membrane receptors that sense extracellular microbes and trigger antipathogen signaling cascades. More recently, intracellular microbial sensors have been identified, including NOD-like receptors (NLRs). NLRs detect/sense conserved structures of the microorganisms, the pathogen-associated molecular patterns (PAMPs). PRRs activate intracellular signals that collaborate for efficient activation of host defense. One such specific collaboration is the interaction between TLRs and intracellular NLRs that recognize PAMPs, as well as host-derived danger signals danger associated molecular patterns (DAMPs). Importantly, NLR members are involved in the assembly of molecular platforms, the inflammasomes, activated upon cellular infection, or stress that trigger the maturation of proinflamma
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