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IAIS Abstracts Melbourne 2005 Book of Abstracts List of Committees Organising Committee Steering Committee Chairs Ian Adcock, UK John Hamilton, Australia Ian Ahnfelt-Ronne, Denmark Eric Morand, Australia Gareth Bowen, UK Michel Chignard, France Gary Anderson, Australia John Hamilton, Australia Gareth Bowen, UK Gordon Letts, USA Andrew Cook, Australia Lisa Marshall, USA Michael Hickey, Australia Tineke Meijers, Canada Gordon Letts, USA Tatsutoshi Nakahata, Japan Alan Lewis, USA Wim van den Berg, The Netherlands Lisa Marshall, USA Kouji Matsushima, Japan Amy Roshak, USA Glen Scholz, Australia Ross Vlahos, Australia Young Investigator Award Committee Program Committee Chair: Chair: Glen Scholz, Australia Michael Hickey, Australia Laurent Audoly, Canada Andrew Cook, Australia Susan Brain, UK John Hamilton, Australia John Schrader, Canada Lisa Marshall, USA Vincent Lagente, France Eric Morand, Australia Kouji Matsushima, Japan Glen Scholz, Australia Ross Vlahos, Australia For enquiries after the Congress please contact the Congress Secretariat: ICMS Pty Ltd Attention: 7th World Congress on Infl ammation 2005 84 Queensbridge Street Southbank Vic 3006 Australia P: +61 3 9682 0244 F: +61 3 9682 0288 E: infl [email protected] W: www.infl ammation2005.com Contents Sunday 21 August 2005 Abstract No. Page Title Morning 1001 — Plenary 1: Peter Doherty 1002 -1004 — Symposium 1: Chronic Obstructive Pulmonary Disease 1005 - 1008 S 85 Symposium 2: Arthritis Afternoon 1010 - 1013 S 85 Focus Group 1: Understanding Infl ammation through Genetics, Genomics and Proteomics 1014 - 1018 S 86 Focus Group 2: Asthma 1019 - 1022 S 88 Focus Group 3: The Immunoregulatory Response 1023 -1027 S 89 Focus Group 4; Structure-Based Drug Design 1028 - 1032 S 90 Focus Group 5: Chronic Obstructive Pulmonary Disease 1033 - 1037 S 90 Focus Group 6: Rheumatic Diseases Monday 22 August 2005 Abstract No. Page Title Morning 2001 S 92 Plenary 2: Marc Feldmann 2002 — Research Highlights: Alberto Mantovani 2003 - 2006 — Symposium 3: Breaking Steroid Resistance 2007 -2010 S 92 Symposium 4: Infl ammation and Regeneration 2011 - 2015 S 92 Focus Group 19: Biomarkers and Imaging Afternoon 2016 – 2021 S 94 Focus Group 7: Cytokines 2022 – 2026 S 95 Focus Group 8; Leukocyte Traffi cking 2027 – 2032 S 96 Focus Group 9: Infl ammation and Cancer 2033 – 2038 S 97 Focus Group 10: Receptors/Signalling 2039 – 2043 S 98 Focus Group 11: Coagulation 2044 – 2049 S 99 Focus Group 12: Young Investigators Tuesday 23 August 2005 Abstract No. Page Title Morning 3001 S 102 Plenary 3: Luke O’Neill 3002 — Research Highlights: Michael Karin 3003 – 3006 S 102 Symposium 5: Macrophages and Infl ammation – The Key to Much Pathology 3007 – 3011 S 103 Symposium 6: Matrix Metalloproteinases in Tissue Remodelling Afternoon 3012 –3016 S 104 Focus Group 13: Signalling in Infl ammation 3017 – 3021 S 105 Focus Group 14 Obesity/Diabetes and Infl ammation 3022 – 3025 S 106 Focus Group 15; Infl ammation in the Central Nervous System 3026 – 3030 S 106 Focus Group 16: Receptors and Innate Immunity 3031 – 3035 S 108 Focus Group 17: Atherosclerosis 3036 – 3039 S 109 Focus Group 18: Renal and Transplantation Immunology Wednesday 24 August 2005 Abstract No. Page Title Morning 4001 –4004 S 110 Plenary 4: Diverse Mechanisms and Impact of Infl ammatory Responses 4005 – 4007 S 110 Plenary 5: Late Breaking Clinical Data on New Anti-Infl ammatory Drugs Please note: No abstracts have been received for some sessions and the session titles are therefore not included in this supplement. Abstract numbers are identical to poster board numbers. Posters will be on board from Sunday 21 August until the conclusion of the Congress on Wednesday 24 August. Abstracts for General Poster Topics Sunday 21 August 2005 Presenters by Boards Abstract No. Page Topic 10:30 – 11:00 12:30 – 13:30 15:30 – 16:00 5001 -5041 S 115 Rheumatic Diseases 5042 – 5062 S 127 The Immunoregulatory Response 5063 - 5067 S 134 Structure-Based Drug Design 5068 - 5087 S 135 Asthma 5088 - 5096 S 141 Understanding Infl ammation Through Genetics and Protemics 5097 - 5106 S 143 Chronic Obstructive Pulmonary Disease Monday 22 August 2005 6001 – 6031, 6033, 6037 S 147 Cytokines 6034, 6036, 6038-6052, 6084 S 156 Receptors/Signalling 6053-6054 S 161 Coagulation 6055-6070 S 162 Infl ammation and Cancer 6032, 6035, 6071-6083, 6085 S 155 Leukocyte Traffi cking 6086-6089 S 171 Diversity of Infl ammation Tuesday 23 August 2005 7001-7044 S 173 Signalling in Infl ammation 7045-7067 S 185 Receptors and Innate Immunity 7068-7076 S 192 Obesity/Diabetes and Infl ammation 7077-7100 S 194 Infl ammation in the Central Nervous System 7101-7120 S 201 Atherosclerosis 7121-7125 S 207 Renal and Transplantation Immunology Young Investigator Award Finalists S 212 Introduction Mini Paper 1 2044 S 213 IL-23 Drives The Expansion Of Pathogenic Th IL-17 Cells Required For Autoimmune Infl ammation Mini Paper 2 2048 S 215 Directed Gp130-Mediated Signalling Dissociates Infl ammation From Fibrosis In Bleomycin-Induced Lung Injury Mini Paper 3 2045 S 217 A Novel Role For Annexin 1 In Macrophage Phagocytosis Mini Paper 4 2046 S 219 Signalling Pathway Of TNF-α-Induced AQP3 Expression In Human Gingival Epithelial Cells: Implications In The Pathogenesis Of Periodontitis Mini Paper 5 2047 S 221 Joint Damage And DC Function During Rheumatoid Arthritis Is Strictly Controlled By Fc Gamma Receptor Iib Mini Paper 6 2049 S 223 Immune Complexes Alter Cerebral Microvessel Permeability: Roles Of Complement And Leukocyte Adhesion Author Index S 225 Plenary Talks, Symposia and Focus Groups Infl amm. res. Supplement 2 (2005) Sunday 21 August 2005 S 85 1006 1012 Signalling Platforms that Mediate the Infl ammatory Response RNAi library screening based approaches to target identifi cation for Infl ammatory Diseases Christopher A McCulloch, University of Toronto, Canada Moitreyee Chatterjee-Kishore, Wyeth Research, United States IL-1-induced signals may serve in host defense or, paradoxically, contrib- ute to infl ammatory tissue injury in arthritis, periodontitis and lung fi brosis. Whole genome transcriptional and proteomic profi ling efforts that help IL-1 stimulates Ca2+ release and expression of the early response genes identify novel signaling pathway components and targets are powerful c-fos and c-jun as well as multiple cytokines and infl ammatory factors tools for drug discovery. However, much of the data obtained from expres- that drive extracellular matrix degradation via mitogen activated protein sion profi ling experiments provides information about genes and proteins kinase pathways. IL-1-induced signaling in fi broblasts and synoviocytes whose expression correlates with a functional phenotype. RNAi technol- requires the formation of protein complexes in spatially restricted cellu- ogy has emerged as a revolutionary new method of targeted gene silencing lar domains termed focal adhesions. Peptides based on the structure of and can greatly accelerate the process of gene functionalization and help the anti-adhesive domains of tenascin, osteonectin and thrombospondin validate the role of genes in causation of the phenotype under study. In the cause dispersion of focal adhesions. These peptides also block IL-1-in- last two years, libraries of chemically synthesized (siRNA) or expressed duced calcium fl uxes and ERK (but not JNK or p38. We have found that (shRNA) gene knockdown reagents have been developed and used to di- the protein tyrosine phosphatases PTP-alpha and SHP-2 are enriched in rectly identify genes which when knocked down directly affect phenotypes focal adhesions and there regulate IL-1-induced calcium signaling. This of interest. signaling pathway is dependent on the association of SHP-2 with PLC- We are using the power of RNAi library based gene knockdown to iden- gamma 1. We also found that the endoplasmic reticulum proteins calnexin tify genes that are of direct relevance to various infl ammatory phenotypes. and calreticulin physically associate with focal adhesions. Focal adhesion- Initial hits from these screens are then prioritized using expression and endoplasmic reticulum interactions are required for calcium release from functional profi ling and classifi ed using literature-mining tools such as In- the endoplasmic reticulum and subsequently, for activation of ERK. As genuityTM. Details of the RNAi library screening workfl ow and examples Ras signaling to ERK involves sequestration of Ras to endoplasmic re- of analysis of siRNA library screen data using various molecular profi ling ticulum membranes, the co-localization of focal adhesions with the endo- techniques will be presented. plasmic reticulum provides an attractive mechanism for optimizing signal transduction. We suggest that the spatial approximation of these organelles creates molecular staging sites for the effi cient conversion of upstream 1013 IL-1 signals into the activation of the protein kinase pathways that lead ultimately to ERK activation. Two Novel, Highly Upregulated Nuclear Factors in Infl ammation Natasha C Foster, Centre for Immunology, St Vincents Hospital, Sydney, 1010 Australia Kristina Warton, Centre for Immunology, St Vincents Hospital, Sydney, ENU mutagenesis based screens Australia Wendy A Gold, Centre for Immunology, St Vincents Hospital, Sydney, Matthew Cook1,2, Carola Vinuesa1, Keats Nelms2, Chris Goodnow1,2 Australia Australian National University1 and Phenomix Australia2, Canberra ACT. Keith K Stanley, Centre for Immunology, St Vincents Hospital, Sydney, Australia Treatment for autoimmune diseases such as systemic lupus erythemato- sus and rheumatoid arthritis (RA) with global immunosuppression is often The aim of this study was to characterise two novel genes induced by pro- unsuccessful and frequently associated with side effects. Improved treat- infl ammatory cytokines in human endothelial cells. Both genes are up- ment will depend on targeting more precisely the key pathogenic path- regulated over 30 fold following treatment with IL-1?. They correspond ways. Strategies to identify the genetic basis of these pathways include to separate genes located less than 100kb apart on the same chromosome, investigation of mice with rare spontaneous mutations that give rise to and they share 78% homology at the amino acid level.
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