Mechanisms of Lymphocyte Activation and Immune Regulation X: Innate Immunity PDF
Preview Mechanisms of Lymphocyte Activation and Immune Regulation X: Innate Immunity
MECHANISMS OF LYMPHOCYTE ACTIVATION AND IMMUNE REGULATION X Innate Immunity ADVANCES IN EXPERIMENTAL MEDICINE AND BIOLOGY Editorial Board: NATHAN BACK, State University of New York at Buffalo IRUN R. COHEN, The Weizmann Institute of Science DAVID KRITCHEVSKY, Wistar Institute ABEL LAJTHA, N. S. Kline Institute for Psychiatric Research RODOLFO PAOLETTI, University of Milan Recent Volumes in this Series Volume 553 BIOMATERIALS: From Molecules to Engineered Tissues Edited by Nesrin Hasırcı and Vasıf Hasırcı Volume 554 PROTECTING INFANTS THROUGH HUMAN MILK: Advancing the Scientific Evidence Edited by Larry K. Pickering, Ardythe L. Morrow, Guillermo M. Ruiz-Palacios, and Richard J. Schanler Volume 555 BREAST FEEEDING: Early Influences on Later Health Edited by Gail Goldberg, Andrew Prentice, Ann Prentice, Suzanne Filteau, and Elsie Widdowson Volume 556 IMMUNOINFORMATICS: Opportunities and Challenges of Bridging Immunology with Computer and Information Sciences Edited by Christian Schoenbach, V. Brusic, and Akihiko Konagaya Volume 557 BRAIN REPAIR Edited by M. Ba¨hr Volume 558 DEFECTS OF SECRETION IN CYSTIC FIBROSIS Edited by Carsten Schultz Volume 559 CELL VOLUME AND SIGNALING Edited by Peter K. Lauf and Norma C. Adragna Volume 560 MECHANISMS OF LYMPHOCYTE ACTIVATION AND IMMUNE REGULATION X: Innate Immunity Edited by Sudhir Gupta, William Paul, and Ralph Steinman Volume 561 CHEMISTRY AND SAFETY OF ACRYLAMIDE IN FOOD Edited by Mendel Friedman and Don Mottram A Continuation Order Plan is available for this series. A continuation order will bring delivery of each new volume immediately upon publication. Volumes are billed only upon actual shipment. For further informa- tion please contact the publisher. MECHANISMS OF LYMPHOCYTE ACTIVATION AND IMMUNE REGULATION X Innate Immunity Edited by Sudhir Gupta University of California Irvine Irvine, California William E. Paul NIAID, NIH Bethesda, Maryland and Ralph Steinman Rockefeller University New York, New York Library of Congress Cataloging-in-Publication Data Gupta, Sudhir. Mechanisms of lymphocyte activation and immune regulation X: innate immunity/ Sudhir Gupta, William E. Paul, Ralph Steinman. p. cm. (Advances in experimental medicine and biology; vol. 560) Includes bibliographical references and index. ISBN 0-387-24188-4 1. Natural immunity—Congresses. 2. Lymphocyte transformation—Congresses. 3. Immune response—Regulation—Congresses. I. Paul, William E. II. Steinman, Ralph. III. Title. IV. Series. QR185.2.G87 2005 616.07(cid:2)9—dc22 2004065389 A C.I.P. Catalogue record for this book is available from the Library of Congress. Proceedings of 10th International Conference on Mechanisms of Lymphocyte Activation and Immune Regulation: Innate Immunity, held February 6–8, 2004 in Newport Beach, California ISSN: 0065 2598 ISBN-10: 0-387-24188-4 ISBN-13: 978-0387-24188-3 (cid:2)2005 Springer Science(cid:2)Business Media, Inc. All rights reserved. This work may not be translated or copied in whole or in part without the written permission of the publisher (Springer Science(cid:2)Business Media, Inc., 233 Spring Street, New York, NY 10013, USA), except for brief excerpts in connection with reviews or scholarly analysis. Use in connection with any form of information storage and retrieval, electronic adaptation, computer software, or by similar or dissimilar methodology now known or hereafter developed is forbidden. The use in this publication of trade names, trademarks, service marks and similar terms, even if they are not identified as such, is not to be taken as an expression of opinion as to whether or not they are subject to proprietary rights. Printed in the United States of America 9 8 7 6 5 4 3 2 1 springeronline.com ECAFERP Immunological science is an ever expanding enterprise in which wen vistas continually open. Indeed, immunology represents one fo the major scientific crossroads, linking human disease and fundamental biology. Yet even in a field as vigorous as this, the revolution touched off by the demonstration that the nature of innate immune responses determines the quality and the intensity fo the adaptive response has been almost unprecedented. Charles Janeway's prescient presentation at Cold Spring Harbor in ,9891 in which he argued that there were receptors on critical cells in the immune system that were specific for certain invariant ligands expressed by microbial pathogens, planted a seed that has yielded a bumper crop. When he and Medzhitov showed that the Drosophila toll had a vertebrate homolog in the TLRs and that the TLRs were the (or one fo the families of) pattern recognition receptors (PRRs) that eh had postulated, there was no stopping the flood fo highly innovative and important research that followed. Eleven different TLRs have been identified and the list oftheir ligands grows. Other molecules, some known for a long time, can also be validly considered .sRRP The cellular and molecular details fo how pathogens are detected by the immune system and how that detection is translated into the mounting of an immune response appropriate in quality to the lifestyle (disease style) of the pathogen are being rapidly unraveled. In many respects, this newly recognized driht" law fo immunology" - the innate immune response directs the adaptive response - has established itself fully beside the first law (universality of immune recognition) and the second law (avoidance of selfreactivity). The Tenth International Conference on Lymphocyte Activation and Immune Regulation, part fo the biennial series held at Newport Beach California, dealt with this critical area. The presentations revolved about the topic fo innate immunity, which was the title fo the conference. Many fo the leading figures in research in this subject were present. The presentations represented the cutting edge fo contemporary research and inspired a spirited and highly useful discussion. This volume, representing the papers that summarize the lectures, should provide the reader with a very good picture fo this field in the midpoint fo the first decade fo the 21st century. The meeting and the book are organized along the main themes fo the field, Toll Receptors and TLRs, NK cells, Dendritic Cells, and the Complement System. Rather than reviewing the contents fo the individual chapters, which the reader can do at hisher leisure, we emphasize the fact that this is a field in flux. Much has been iv PREFACE accomplished but the field has yb no means become ".erutam" Areas fo major con- progress exist; troversy is rapid; today's certainty yam eb the concept on dust tomorrow's .paeh this say only can We to the :redaer tuned, stay ts eebht is yet to come. The organizers are particularly grateful to all ohw played a role ni making the meeting a success and the book a reality. We particularly thank Janet Nagurski for assistance. editorial Gupta Sudhir William .E Paul Ralph Steinman STNETNOC 1. TIR GNINIATNOC-NIAMOD SROTPADA ETALUGER TLR GNILANGIS SYAWHTAP ................................................................ Masahiro and Yamamoto Shizuo Akira .2 TOLL-LIKE GN I:KSNRIOLTPECER ETANNI DNA EVITPADA YTINUMMI ..................................................... Chandrashekhar Pasare Ruslan and Medzhitov .3 NOITAVITCA OF TCESNI DNA ETARBETREV TOLL :GNILANGIS MORF SUONEGODNE ENIKOTYC DNAGIL TO DIRECT NOITINGOCER OF SNRETTAP NEGOHTAP ......................... Nicholas .J Alexander Gay, .N R. Monique Gangloff Weber and .4 GENETIC SISYLANA OF :YTINUMMI ETANNI IDENTIFICATION DNA NOITCNUF OF TITRH E RETPADA PROTEINS ...... Beutler, Bruce Kasper Hoebe, Philippe Georgel, Koichi Tabeta, Xin and Du 5. ,BK-FN NA YLIRANOITULOVE DEVRESNOC ROTAIDEM OF ENUMMI DNA YROTAMMALFNI SESNOPSER ...................................................................... Xiao and Changchun Sankar Ghosh 6. ECNEULFNI OF KIR YTISREVID NO NAMUH YTINUMMI .......................................................................................................... Peter Parham 7. D2GKN NI ETANNI DNA YTINUMMI EVITPADA Lewis .L Lanier ...................................................................................................... 8. SPECJFIC DNA CI'FICEPS-NON LARUTAN KILLER CELL SESNOPSER TO LARIV INFECTION ............................................................................................ Wayne .M Yokoyama viii STNETNOC 9. GNISSECORP NEGITNA DNA NOITATNESERP YB DENDRITIC :SLLEC CELL SMSINAHCEM LACIGOLOIB ............................................................................................................ Ira Mellman 63 10. NAMUH THYMIC LAMORTS TRIGGERS LYMPHOPOIETIN DENDRITIC DETAIDEM-LLEC ALLERGIC NOITAMMALFNI DNA +4DC CELL T CITATSOEMOH NOISNAPXE .................................... Norihiko Watanabe, Vassili Soumelis, and Yong-Jun Liu 69 11. ROLE OF 6FART NI THE ENUMMI METSYS ....................................................................................................... Yongwon Choi 77 12. THE ETANNI SNOITCNUF OF CELLS DENDRITIC NI PERIPHERAL SEUSSIT DIOHPMYL Ralph .M Bonifaz, Laura Shin-ichiro Steinman, Liu, Fujii, Kang David Maggi Bonnyay, Yamazaki, Hawiger, Pack, Daniel Sayuri .................................. Tomonori lyoda, Michel and Inaba, Kayo .C Nussenzweig 83 13. THE GNIDNIB-ESONNAM :NITCEL NA INFECTION ENEG YTILIBITPECSUS ............................ .R Alan Lei Ezekowitz, Shi, lain Fraser, and Kazue Takahashi 99 14. YPAREHTONUMMI AIV CELLS DENDRITIC .A Laupeze, Caroline Hiroaki Beatrice Saito, Palucka, Karolina Aspord, Paczesny, Jego, Joseph Sophie Gaetan Fay, Virginia Pascual and ............................................................................................... Jacques Banchereau 105 15. YNEGOTNO OF SNAHREGNAL CELLS DNA GRAFT SUSREV TSOH ESAESID ..................................................................................................... Miriam Merad 115 16. ROLE OF THE 91DC DNA 53112DC RECEPTOR NI XELPMOC ,YTINUMMI ETANNI ESNEFED TSOH DNA YTINUMMIOTUA .................................................................. Karen .M Haas Thomas and .F Tedder 125 17. ROLE OF TNEMELPMOC 2 RECEPTOR NI THE SISENEGOHTAP OF CIMETSYS SUPUL SUSOTAMEHTYRE ................................................................................................... Susan .A Boackle 141 18. COMPLEMENT NOITALUGER YCNANGERP GNIRUD ........................................................................................................ Molina Hector 149 XEDNI .......................................................................................................................... 157 GNINIATNOC-NIAMOD RIT SROTPADA ETALUGER RLT GNILANGIS SYAWHTAP orihasaM ~amamoto' dna ouzihS ~kira"' .1 NOITCUDORTNI Against invading ,smsinagroorcim vertebrates including mammals develop innate immune systems, hcihw are activated yb microbial components possessing conserved structures called negohtap associated molecular patterns (PAMPs); including bacterial cell llaw components, dna lariv genomic AND dna .ANR PAMPs are recognized yb pattern recognition receptors ylniam expressing on immune responsive cells. Toll-like receptors "')SRLT( are an example fo pattern recognition receptors, and TLR family conserved are members .slammam gnoma To date, 10 and 12 reported been have TLRs ni have TLRs all Almost respectively. mouse, and human neeb PAMPs; recognize to shown TLR2 is the receptor for nacylgoditpep dna lipoprotein, including bacterial lipoprotein (BLP) and mycoplasmal lipoprotein ."')2-PLAM( Especially, BLP and MALP-2 are reportedly recognized in the functional heterodimeric association fo TLR2 htiw TLRl and TLR6, TLR4 respectively. is involved ni recognition the fo wall cell gram-negative a lipopolysaccharide component, .',~)SPL( TLR5 is for flagellin, receptor a a component fo bacterial .8allegalf TLR3 dna TLR9 are receptors for double-stranded (ds) ANR dna unmethylated CpG ,AND hguohtlA the natural ligand for TLR7 is yet to eb the receptor identified, ne esbah imidazoquid or its to recognize derivative, shown -R .848 Since yeht are dezilitu in the treatment fo genital warts caused yb namuh papilomavirus, the ligand for 7RLT seems to be a component fo .'1sesuriv Thus, accumulating evidence ylraelc demonstrates that TLRs serve as pattern recognition 1). (Figure microbes invading detect to receptors tnemtrapeD' of tsoH ,esnefeD hcraeseR lai be otrruoctfiiMtsnI Diseases, akasO .ytisrevinU ,OTARE' 1-3 ,ako-adamaY atiuS akasO 565-0851, .napaJ ecnednopserroC dluohs eb desserdda :ot ouzihS ,arikA tnemtrapeD of tsoH ,esnefeD laiborc irM oeftutit shncIraeseR ,sesaesiD akasO 1-3 ,ytisrevinU ,ako-adamaY atiuS akasO 565-0851, ;napaJ :enohp ;3038-9786-6-18 :xaf ;5038-9786-6-18 :liam-E .pj.ca.u-akaso.nekib@arikas Mechanisms oj'lymphocvte Activation and Immune Replation X detidE yb atpuG et a/. ,r,egnirpS 2005 TIR ETALUGER SROTPADA SIGNALING TLR SYAWHTAP - Lipoprotein Unrnethylated MALP-2 BLP PON Flagellin R-848 CPG DNA LPS drRNA erugiF 1. Summary fo PAMPs that era dezingocer by TLRs .2 EHT DNA SYAWHTAP TNEDNEPED-SSDYM THE -SSDYM TNEDNEPEDNI SYAWHTAP sA a structural feature, lla TLRs ssessop an extracellular domain rich in leucines, repeat the leucine-rich called dna ,)RRL( na intracellular hcih wniamod substantial shows ygolomoh htiw portion the intracellular fo IL-1 receptor (IL-1R) members, family eht so called Toll-IL-1R (TIR) domain. RRL has neeb shown ot be responsible for the interaction htiw PAMPs. Ligation fo the extracellular domain fo TLRs with microbial components activates intracellular signaling cascades, culminating ni various immune dendritic and proliferation cell B production, cytokine proinflammatory as such responses cell (DC) maturationL3. The signaling cascades originate from the TIR domain, hcihw recruits an intracellular TIR domain-containing adaptor molecule, MyD88 (meloid a), Differentiation factor hcihw saw yllanigiro identified as a myeloid differentiation yramirp rapidly is that gene response no pduetaluger-pu differentiation IL-6-stimulated fo MI myeloleukemic cells into macr~~ha~es'~. Subsequent in vitro studies showed overexpression fo MyD88 leads to activation fo BK-FN dna MAPKS'~"~. MyD88 possesses a RIT domain ni the portion C-terminal dna a Death Domain (DD) in the -N lanimret portion, hcihw interacts htiw gniniatnoc-DD kinases such as IL-1R-associated members. family (IRAK) kinase ,me hgtnomA IRAK-1 4-K AdRnIa to been have shown participate in activation fo R1-LI dna TLR-mediated signaling pathways. Ligation fo ht iswPMAP TLRs to leads phosphorylation fo 1-KARI dna and IRAK-4, neht activates BK-FN dna sKPAM via TRAF~"-". Evidence provided from studies gnisu mice gene-targeted clearly demonstrates the significance fo MyD88 ni the activation fo RLT signaling pathways. MyD88-deficient mice showed completely defective responses to IL-1 family members ni terms fo gene expression dna activation fo signaling molecule^'^. to responses Moreover, TLRI, TLR2, ,SRLT TLR6, 7RLT dna TLR9 ligands were also completely abolished in MyD88- indicating cells, deficient taht MyD88 is na those for adaptor essential re~e~tors""'"~~~'.
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