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  • 1. Newsletter of the International Cytokine Society Year 2002, issue no.1 In this issue: 0001. The Newsletter goes electronic. From this issue, the Newsletters will only be published electronically. It will be available on the ICS website and sent by e- mail to ICS members who have given the ICS their e-mail addresses: this is a good time for you to send it or update it if we don’t have it. 0002. Observer, by Byron H. Waksman. 0003. Side-effects of anti-TNF therapy? Charles A. Dinarello. 0004. The 2002 Cytokine Meeting in Torino. xxxx Announcements. ICS Life time membership to Drs. Metcalf and Sachs. At the Hawaii meeting, the 2001 lifetime membership of the ICS was awarded to Donald Metcalf and Leo Sachs. Drs. Metcalf and Sachs have characterized the differentiation of bone marrow precursors into mature blood cells. Their studies led to the identification of colony-stimulating factors, among the first cytokines to be described and the most used clinically. xxxx The Newsletter goes electronic The Newsletter will, from this issue on, be sent only in electronic format and posted on the ICS Website: (http://bioinformatics.weizmann.ac.il/cytokine/) All ICS members and those who wish to receive the Newsletter please send their e-mail address to the ICS office in the USA by fax (706) 722-7515 or e-mail (maps@csranet.com), or to the Editor. The Newsletter will also be sent to all members of the European Cytokine Society thanks to the effort of Didier Fradelizi. xxxx
  • 2. Observer Concept and method For young investigators, it may seem obvious that one does research to answer questions, important questions if possible. This goal gets muddled by the fact that, to answer any question of interest today, one has to apply complex techniques, many of which are already out there. Companies furnish kits and supply reagents, which make it easier to answer questions and save the investigator the trouble of devising new methods and/or making reagents on his own. This fact, however, tends to make the technique, in some instances, seem more important than the question and to obscure the continued emergence of significant questions that can be solved by less complex, if older, methods. A further inevitable consequence is that research done with older methods, and more than 5 years ago, is considered of doubtful value or is not considered at all. Immunologic technology (cellular and humoral), in the early part of the century, was largely limited to the study of whole animals and of immunopathologic reactions in such organs as kidney, heart, lung, brain, eye, etc; or of plasma and its constituents, antibody, complement, and mediators such as histamine. In the mid-30’s, Karl Landsteiner, a highly innovative investigator, created a simple new technology, the adoptive transfer of lymphoid cells, in an attempt to find the mediator of delayed (tuberculin-type) hypersensitivity and, by extension, of immunologically determined inflammatory tissue lesions in tissues other than skin. Elvin Kabat, equally innovative and working almost at the same time, combined conventional protein separation techniques with ultracentrifugation (a method newly devised by T. Svedberg) and electrophoresis (devised by A. Tiselius) to identify antibodies as immunoglobulins of a certain molecular size and charge. Here we see, in the one case, that a creative scientist can devise a new method to answer an outstanding question or, in the other, that he can use emerging technology for this purpose. A decade later, Fagraeus’ innovative use of cell culture and Coons’ invention of the immunofluorescence technique, with the beginning application of cell markers, provided a decisive identification of the plasmacyte as the cell making antibody. The earlier protein separation methods and proliferating techniques for chromatographic and electrophoretic separation in solid media, such as paper, starch, agar, polyacrylamide gel, and ultimately cellulose acetate and the like found immunologic application in Oudin, Ouchterlony, and Grabar’s hands with the separation of isotypes, allotypes, and idiotypes of immunoglobulins and the dissection by Mayer, Pillemer, Ecker and their colleagues of the complement system. It is apparent that the technical limitations did little to inhibit discovery. By 1960, the distinction between cellular and humoral immunity was fully established. The role of the lymphocyte as the central cell of immunology was convincingly demonstrated, and many important models of immunologically mediated autoimmune disease, affecting the eye, the CNS, the PNS, the thyroid, pancreas, 2
  • 3. and adrenal had been described. Yet think of this: before 1960, there was no disposable glassware, inbred strains of animals were not in general use, nor were there well established techniques for culturing lymphoid cells. The use of isotopes and of immunofluorescence were in their earliest stages and there were, of course, no radioimmunoassays and no kits. There were also no lines or clones of cells. Even purified proteins like ovalbumin were unavailable - you had to make your own. These limitations were not reflected in the importance of the discoveries being made. I am, of course, also making a distinction between the simplicity (the starkness, one might almost say) of those times and today’s complexity. That contrast applies, as well, to what one may call the mechanical/administrative/bureaucratic aspects of science. Most scientific articles had a single author or two authors, rarely three, and new immunological research had to be published in the Journal of Immunology or the Journal of Experimental Medicine (or Science or Nature) or in specialty journals like the British Journal of Experimental Pathology, the Journal of Investigative Dermatology, or the Journal of Neuropathology and Experimental Neurology. The only significant review series were Physiological Reviews and Progress in Allergy. The meetings of the American Association of Immunologists, always part of the FASEB meeting, were the only game in town; small, elite meetings virtually did not exist (or were limited to the Gordon Conferences). The AAI meetings were themselves small, elite meetings. Research was in whole animals, or bacteria or Drosophila. Yet one could breathe, one could explore. After 1960, the technological limitations were still severe. T and B cell lines and clones had not been invented and polyclonal lymphocyte populations were the usual subjects of study. Cell sorting techniques lay in the future. APC, when these were considered at all, were macrophage populations that must surely have been contaminated with dendritic cells of various types. The T cell that was studied was the TCR αβ T cell, with a distinction made between helper and cytotoxic functions and later between CD4 and CD8 subsets. Unusual cells, such as γδ T cells, NK cells, NK T cells, DN T cells, TCR αα Tcells, IEL, and the CD25+CD4+ suppressor T cell, were not thought of at all. In this period, cells were stimulated in vitro with mitogens (plant lectins, LPS) acting on what are now recognized as Toll family receptors of the innate immune system; since the TCR was still unknown, the use of anti-CD3 for polyclonal T cell stimulation, so common today, could not be envisaged. The study of antigen/epitope specific systems required the use of whole animals, except for the MLR, which was specific and was large enough to be easily measured. Anti- idiotypic T cell stimulation was unknown as was stimulation via the Fc receptor, KIR, and the like. Proliferation and cytotoxicity were the commonly used readouts of cell stimulation experiments. "Cytokine profile" was an unknown concept; indeed most major CK (cytokines) after IL- 1, lymphotoxin and TNF, and MIF (macrophage migration inhibitory factor, now thought to be mainly γ interferon) were yet to be discovered. 3
  • 4. Yet, in spite of these limitations, the period between 1960 and 1970 witnessed a host of fundamental discoveries. Anyone who has read Rabelais has taken delight in his long outrageous lists of things; our topic is best illustrated from this point on with Rabelaisian lists. Here are a few: the discovery of the central lymphoid organs, bone marrow, thymus, bursa of Fabricius (and MALT as the probable mammalian equivalent); the discovery that the thymus is a major site, or the major site of specific immunologic tolerance; the description of T and B lymphocytes; the recognition of CK as mediators of inflammation; the use of newly devised cell culture methodologies, first, to establish the basic reactions underlying specific cell-mediated immune reactions, notably proliferation, the helper function, cytotoxicity, and CK secretion and, second, to study cell interactions in antibody formation; use of the newly invented PFC (plaque- forming cell) method to enumerate antibody-forming cells (note that this method was not yet successfully applied to T cells). In the next decade, one had the first the use of cell markers, e.g. to distinguish CD4+ and CD8+ T cells; the discovery of "suppressor T cells," now delicately referred to as "regulatory cells;" the role of CK in both help (cell cooperation) and regulation (suppression); the relationship between "immune response genes," the MHC, antigen processing and presentation, and "dual recognition;" network concepts based on idiotopes and anti-idiotypic recognition, cooperation and suppression, and CK; and molecular mimicry, to name a few. 1980 marks a technological watershed in immunologic research, with the introduction of molecular biology, cell and molecular cloning, and the growing exploration of genetic and phylogenetic relationships. The cloning of T lymphocytes may be said to have changed the face of immunology forever. Ever more refined structural studies of immunoglobulins, the T cell receptor, the MHC, adhesion molecules, various cytokines (and later chemokines) and their receptors were paralleled by the descriptions of Thl/Th2 and Tcl/Tc2 relationships, and an increasing appreciation of the hitherto black box of neuro- immuno-endocrine relationships, including several startling discoveries: that some cytokines can act as neurotransmitters and some lymphocytes make hormones, such as ACTH, and that genetically determined differences in the neuroendocrine axes (HPA, HPT, and HPG) can affect the character of immune inflammatory responses. The accelerated pace of new discovery was now matched by the rapid increase in profitable applications of the latest findings, the growth of biotech companies, and the increasing invasion of fundamental research by company people, company funding, and quasi-fundamental company ideas, abetted by the difficulty experienced by even the most committed academic scientists in getting grants. The "mechanical/administrative/bureaucratic" aspects of research, furthermore, had not diminished - rather they increased. Since 1990, the study of signaling pathways and regulation at the molecular level have become dominant, and we are experiencing a flood of new technologies and 4
  • 5. far too many new discoveries to be chronicled in this short account. Think, for example, of the implications of "altered peptide ligands" in their interactions with T cells, the complexities of dendritic cell research, or the different subsets of yd T cells, presentation of glycolipid and microbial peptide epitopes by the many new forms of MHC, the strange ways of NK T cells. At the same time, new methods and the commercial drive to see them used are driving the research machine to an ever-increasing extent. Much of today’s research is conceived in terms of what you can do with chips bearing microarrays rather than what fundamental problems remain to be solved. An inevitable offshoot of complexity is specialization, with the implication that kidney specialists need not know the latest developments in brain research, investigative dermatology, or ophthalmology. Before 1960, this specialization interfered with communication among those doing immunologic research, most of whom thought of themselves as internists, neurologists, and the like, rather than immunologists. However, this point is equally apposite for contemporary immunologists. Students of T cell signaling feel they do not need to know the intricacies of the complement cascade or, for that matter, of brain research. Specialization is followed in due course by "interdisciplinary studies" since most interesting problems, after all, do not come with defined disciplinary/specialty boundaries. It is easy to understand why it sometimes is easier to hang your hat on a method than to pursue a conceptual problem through all the relevant disciplines. Scientists - and this comment applies especially to scientists at the earliest stage of their careers - must somehow, in the face of the "flood" of new techniques and new discoveries as well as the limits imposed by specialization, acquire a meaningful perspective on what research problems are most important and what kind of research they may hope to accomplish. The balancing act between concepts and methods is seen best in some of the outstanding papers of earlier decades, to be read by young and old alike while "keeping up with the literature." Byron H. Waksman, 9/4/2001 xxxx Anti-TNF therapy, by Charles Dinarello Concern about the effect of chronic cytokine blockade was flashed on the screen for an entire day on CNN despite the dominance of news on the events surrounding September 11th and its sequelae. The newsflash had its origins in a paper in the New England Journal of Medicine on the increase number of cases of tuberculosis in patients receiving antibodies to tumor necrosis factor-α (1). Although the increase incidence of tuberculosis (actually reactivation) has been followed in the rheumatoid arthritis community, the importance of the paper’s message will certainly spark discussion among cytokinologists. 5
  • 6. To date 150,000 patients worldwide have received the chimeric monoclonal antibody against human TNF-a called infliximab; some have been patients with rheumatoid arthritis whereas others have been patients with Crohn’s disease. In addition, anti-TNFa therapy is being used in patients with psoriasis and Wegener’s granulomatosis. The use of other antibodies to TNF-a are also associated with increased risk of reactivation tuberculosis, but the use of a soluble form of the p75 TNF receptor (called etanercept) is not associated with the increase in tuberculosis. However, an increase in other opportunistic infections has been reported with the use of etanercept. From the early days of cytokine research, even before molecular cloning and availability of recombinant cytokines, the issue of “bad guy” versus “good guy” cytokine was a topic of interest and research. The cytokines that were discussed 20 years ago in this regard were IL-1 and TNF. Now, the issue of whether these same cytokines are detrimental to the host or needed by the host for survival is no longer an issue for the laboratory animal but have entered the clinical arena. At first, there was a great deal of excitement that blocking IL-1 or TNF would rescue patients at risk for death during severe sepsis or septic shock (also known as systemic inflammatory response syndrome or SIRS). Despite overwhelming data in animal models that blocking IL-1 or TNF would protect animals from lethal endotoxemia, there was no dramatic improvement in the 28 day all- cause mortality when blocking IL-1 or TNF was used in humans with sepsis or septic shock. In several double-blind, placebo-controlled randomized studies involving over 10,000 patients, the whole field of anti-cytokine therapy for treating disease nearly collapsed, several biotech companies went out of business and big pharmaceutical companies lost hundreds of millions of dollars. In contrast, there has been an impressive and in some cases dramatic improvements in the reduction of the severity of rheumatoid arthritis using the same agents that had no significant effect in reducing mortality in septic patients (2-4). In fact, one agent, a construction of two identical chains of the extracellular domains of the p75 TNF receptor linked to the Fc domain of IgG (generically termed etanercept) actually increased mortality in a dose-dependent fashion in a sepsis trial (5). However, etanercept is used by over 100,000 patients with rheumatoid arthritis either alone or in combination with methotrexate (6) with considerable success. Antibodies to TNFα (infliximab or D2E7) are also used in combination with methotrexate (7, 8). In addition, patients with Crohn’s disease also are treated with infliximab. Patients with ankylosing spondylitis and psoriatic arthritis also have been successfully treated with either etanercept or infliximab. Therefore, it is estimated that 250,000 patients are presently receiving some form of therapy for reducing TNF activity with either the p75 soluble receptor or monoclonal anti-TNFα antibodies. Moreover, rheumatoid arthritis and Crohn’s disease are chronic diseases and treatment is therefore chronic. Anti- cytokine therapies for rheumatoid arthritis do not “cure” the patient of the fundamental autoimmune disease process since upon cessation of anti-cytokine therapy, the disease activity returns. PG: Charles, exactly how many patients receiving anti-TNF therapies have experienced a serious infection? CD: In the United States and Europe, physicians are not legally required to report serious adverse event. An example of a serious adverse effect is pneumonia which requires 6
  • 7. parenteral antibiotics and hospitalization. Reactivation of tuberculosis is also a serious adverse event. During controlled clinical trials of anti-TNF therapy, all adverse events are reported. Therefore, one can read about the incidence of infections with anti-TNF therapy in peer reviewed journals (9). In general, the results are quite favorable in that the incidence of infections are not more than that expected in patients with this disease. However, once a drug is approved by the regulatory agencies, there is no legal requirement to report adverse events and the real incidence of events remains unknown. Reporting an adverse event requires time and documentation and therefore if pneumonia associated with anti-TNF therapy resolves, it is likely that this will not be reported. PG: Besides the paperwork, is there another reason why reporting is thought to be low? CD: In addition, some physicians are reluctant to report serious adverse effects to the regulatory agencies because the data may be used against the treating physician in a medical malpractice lawsuit. As a result, the incidence of infections or cancer in patients receiving chronic anti-TNF therapy may be considerably higher than the present knowledge. PG: What have the regulatory agencies done to advise physicians on the risks of chronic anti-TNF therapies? CD: There are warnings written on the package insert for etanercept and infliximab. These warning labels state that the agents should not be given to patients with infections and stopped if an infection develops. In addition, the new warnings for infliximab state that before starting therapy, all patients should be tested for tuberculosis. That is relatively easy in the United States because Americans do not vaccinate children with BCG and hence Americans are tuberculin skin test negative. In contrast, in Europeans and older Israelis, BCG is used broadly and most patients starting on infliximab will test positive with tuberculin reflecting their vaccination status. PG: Does the increase in opportunistic infections mean the death knell for anti-TNFa therapies? CD: Not at all. These agents have been remarkably successful and have made a major impact on treating two very problematic diseases, rheumatoid arthritis and Crohn’s disease. For many, it is a new life and a reduction in the use of methotrexate and corticosteroids. Of course, not all patients respond to therapies based on blocking TNF but a significant number do. In some patients, the effect is sustained for years. PG: Does the use of IL-1 receptor antagonist (called anakinra) in patients with rheumatoid arthritis have the same association with increased risk of opportunistic infections? CD: To date, no. However, the numbers of patients having received IL-1Ra for rheumatoid arthritis is about 2,000 and although some have been treated for years without opportunistic infections, particularly tuberculosis, we must wait until more patients have been treated. It is important to note that in those patients receiving either infliximab or etanercept, the rapidity of onset of infection to the start of therapy strongly suggests causality and is the most troublesome aspect of the phenomenon. 1. Keane J., S. Gershon, R.P. Wise, E. Mirabile-Levens, J. Kasznica, W.D. Schwieterman, J.N. Siegel, and M.M. Braun. 2001. Tuberculosis associated with infliximab, a tumor necrosis factor-a-neutralizing agent. N Engl J Med 345:1098-1104. 7
  • 8. 2. Elliott M.J., R.N. Maini, M. Feldmann, J.R. Kalden, C. Antoni, J.S. Smolen, B. Leeb, F.C. Breedveld, J.D. Macfarlane, A. Long-Fox, P. Charles, H. Bijl, and J.N. Woody. 1994. Randomised double-blind comparison of chimeric monoclonal antibody to tumour necrosis factor alpha (cA2) versus placebo in rheumatoid arthritis. Lancet 344:1105-1110. 3. Moreland L.W., S.W. Baumgartner, M.H. Schiff, E.A. Tindall, R.M. Fleischmann, A.L. Weaver, R.E. Ettlinger, S. Cohen, W.J. Koopman, K. Mohler, M.B. Widmer, and C.M. Blosch. 1997. Treatment of rheumatoid arthritis with a recombinant human tumor necrosis factor receptor (p75)-Fc fusion protein. N Engl J Med 337:141-147. 4. Bresnihan B., J.M. Alvaro-Gracia, M. Cobby, M. Doherty, Z. Domljan, P. Emery, G. Nuki, K. Pavelka, R. Rau, B. Rozman, I. Watt, B. Williams, R. Aitchison, D. McCabe, and P. Musikic. 1998. Treatment of rheumatoid arthritis with recombinant human interleukin-1 receptor antagonist. Arthritis Rheum 41:2196- 2204. 5. Fisher C., Jr., J.M. Agosti, S.M. Opal, S.F. Lowry, R.A. Balk, J.C. Sadoff, E. Abraham, R.M. Schein, and E. Benjamin. 1996. Treatment of septic shock with the tumor necrosis factor receptor:Fc fusion protein. N Engl J Med 334:1697-1702. 6. Weinblatt M.E., J.M. Kremer, A.D. Bankhurst, K.J. Bulpitt, R.M. Fleischmann, R.I. Fox, C.G. Jackson, M. Lange, and D.J. Burge. 1999. A trial of etanercept, a recombinant tumor necrosis factor receptor:Fc fusion protein, in patients with rheumatoid arthritis receiving methotrexate [see comments]. N Engl J Med 340:253-259. 7. Lipsky P.E., D.M. van der Heijde, E.W. St Clair, D.E. Furst, F.C. Breedveld, J.R. Kalden, J.S. Smolen, M. Weisman, P. Emery, M. Feldmann, G.R. Harriman, and R.N. Maini. 2000. Infliximab and methotrexate in the treatment of rheumatoid arthritis. N Engl J Med 343:1594-1602. 8. Keystone E., M.E. Weinblatt, M. Weisman, D. Furst, H. Paulus, C. Bitbara, S. Fischkoff, and E.K. Chartash. 2001. The fully human anti-TNF monoclonal antibody, adalimumab D2E7, dose-ranging study: the 24 week clinical results in patients with active RA on methotrexate therapy (the ARMADA trial). Ann Rheumat Dis 60 suppl 1:67 (abs). 9. Moreland L.W., S.B. Cohen, S.W. Baumgartner, E.A. Tindall, K. Bulpitt, R. Martin, M. Weinblatt, J. Taborn, A. Weaver, D.J. Burge, and M.H. Schiff. 2001. Long-term safety and efficacy of etanercept in patients with rheumatoid arthritis. J Rheumatol 28:1238-1244. xxxx Newsletter of the International Cytokine society Electronic Edition International Cytokine Society Biotech Park, Suite 9, 1021 15th street, Augusta, GA 30901 Telephone: (706) 722-7511; Fax: (706) 722-7515 E-mail: maps@csranet.com Website: http://bioinformatics.weizmann.ac.il/cytokine/ Officers President: Nancy Ruddle Vice President: Marc Feldman Senior Councilor: Warren Leonard 8
  • 9. Junior Councilor: Mathew Fenton Past President: Jean-Michel Dayer Treasurer: John Hiscott Secretary: Ann Richmond Executive Manager: Sherwood Reichard xxxx This Newsletter is published biannually by the International Cytokine Society. Please submit articles to the Editor: Pietro Ghezzi, Head, Laboratory of Neuroimmunology, "Mario Negri" Institute, via Eritrea 62, 20157 Milano, Italy Fax +39-023546277. Email: ghezzi@marionegri.it Opinions expressed by contributors are not necessarily those of the International Cytokine Society ICS Meetings Cytokines and Interferons 2002 Joint Meeting of the International Cytokine Society (ICS), the International Society for Interferon and Cytokine Research (ISICR), the European Cytokine Society (ECS) and Society for Leukocyte Biology (SLB) Lingotto Congress Center, Torino, Italy October 6-11, 2002 Local Organizing Commitee: Santo Landolfo Gianni Garotta Pietro Ghezzi Alberto Mantovani Josef D. Schwarzmeier Giorgio Trinchieri E-mail: cyto2002@marionegri.it International Advisory National Advisory Committee Committe Anthony Cerami (USA) F. Belardelli (Rome) Jean-Michel Dayer (Switzerland) M. Cassatella (Verona) Charles Dinarello (USA) F. Dianzani (Rome) Janine Doly (France) G. Forni (Turin) Douglas Duff (USA) E. Garaci (Rome) Scott Durum (USA) R. Foà (Rome) Didier Fradelizi (France) L. Moretta (Genoa) David Goeddel (USA) C. Riccardi (Perugia) 9
  • 10. John Hiscott (Canada) S. Romagnani (Florence) Tadamitsu Kishimoto ( Japan) L. Ruco (Rome) Joost Oppenheim (USA) A. Santoni (Rome) Keiko Ozato (USA) L. Varesio (Genoa) Sidney Pestka (USA) Nancy H. Ruddle (USA) Menachem Rubinstein (Israel) Robert Schreiber (USA) George Stark (USA) Tadatsugu Taniguchi ( Japan) Jo Van Damme (Belgium) Jan Vilcek (USA) Stefanie Vogel (USA) Sharon Wahl (USA) David Wallach (Israel) Bryan R.G. Williams (USA) xxxx ORGANIZING SECRETARIAT: M.A.F. Servizi srl - Congress department Via G.B. Vico 7 - 10128 Torino Tel. +39 011 505 900 - Fax +39 011 505 976 www.mafservizi.it E-mail: cyto2002@mafservizi.it Abstract submission Participants are invited to submit abstracts of their work for oral or poster presentation to the Organizing Secretariat, MAF Servizi. Abstracts will be only accepted if sent together with the registration fee within the deadline of 15 June, 2002. The abstracts accepted for oral or poster presentation will be published on the “Journal of Interferon & Cytokine Research” that will be included in the congress kit. Please follow these rules: Fill the TOPICS form you will find inside following page or download it from the congress website www.mafservizi.it and send it together with the file of the abstract by e-mail to pagni@mafservizi.it or by surface mail to the address of MAF Servizi S.r.l. - V. Vico, 7 - 10128 Torino – Italy You could submit the abstract: A) by e-mail pagni@mafservizi.it together with the TOPICS form at point 1) B) on a floppy disk by surface mail including the form at point 1) with the indication of the adopted program topic to the Organizing Secretariat: MAF Servizi srl - Via Vico 7 - 10128 - Torino – Italy 10
  • 11. No abstract form is proposed but please follow the specified details: Language: English Dimension of the sheet of paper: A4 format Borders: 2,5 cm Character: Times 12 Line space: Single Pages: 1 Word Count: About 250 words Abstract deadline: 15 June, 2002 Poster Sessions The dimensions of posters should not exceed the height of 120 cm and the width of 95 cm. Fastening material suitable for light cardboard will be provided. The Authors of accepted posters will be informed about exhibition date and discussion modalities Oral presentation of selected papers (see detailed programme on Workshops) Oral presentations (exposition 10’ + discussion 2’) will be presented on each of the congress days. Within September 20, 2002 authors will be notified if their paper has been selected for oral or poster presentation with the relating schedule. Other technical details Slides must be in standard format (5 cm x 5 cm) and must be submitted to the Slides Center at least 2 hours before the scheduled presentation. Single slide, overhead and direct PC projection will be available in all lecture rooms. GENERAL INFORMATION Congress Venue Torino Lingotto Congress Center V. Nizza 294 - 10100 Torino (Italy) HOW TO REACH TORINO By car Turin lies on the main motorway network (A4, A5, A6, A21). By plane Turin is served by the Torino-Caselle “Sandro Pertini” Airport, located 16 km. from the center of the City. Services are operated on European and domestic flight with daily connections to Amsterdam, London, Paris, Brussels, Zurich, Barcelona, Lisbona, Madrid, Frankfurt, Munich, Dusseldorf, Stuttgard and frequent flight connections to Rome. By train Ralway stations: Torino “Porta Nuova” or Torino “Porta Susa” Turin is connected by train to the rest of Europe through France and Germany. Good connections include Intercity service from Rome, Milan, Venice, Naples. Direct connection from Paris is available by TGV. ORGANIZING SECRETARIAT M.A.F Servizi srl – Congress Division Via G.B. Vico, 7 – 10128 Torino (Italy) 11
  • 12. Phone ++39 011 505.900 Fax ++ 39 011 505.976 e-mail: dpilato@mafservizi.it Registration desk The registration desk will be located in the lobby of the Congress Center and will be open for registration of participants starting from October 6, 2002 at 11:00 a.m. Exhibitors The participation of commercial exhibitors is most welcome. The exhibition area is located along the main branch of the Congress Center, close to main Lecture Hall and along the Poster Area. Further information can be obtained from the Congress Organizing Secretariat, MAF Servizi. Congress Registration Registration for the congress will be possible: 1) by electronic registration form at web site www.mafservizi.it/cytokine2002 or 2) by faxing the registration form to the number ++39 011 505976. All participants are kindly requested to complete the enclosed registration form and to send it to the Organizing Secretariat including the payment. No registration will be accepted without evidence of payment. No registration will be accepted by telephone. Congress Early Registration Fee (VAT included) in Euro: Before 30 May After 30 May Member 700 800 Non Member 800 900 Student 350 400 Accompayning person 130 130 The registration fee for active participants includes: – conference kit – participation in the scientific sessions – abstract book – coffee breaks and Lunch – welcome cocktail and Concert on October 6 – Social Dinner on October 9 The registration fee for Accompayning includes: – welcome cocktail and Concert on October 6 – Social Dinner on October 9 Cancellation Written cancellations must be submitted to the Organizing Secretariat not later than September 7, 2002. In this case 70% of the registration fees will be 12
  • 13. refunded; no cancellation request will be accepted after the above mentioned deadline. Confirmation Within 20 days before beginning of the Meeting and anyway upon receipt of the payment and the registration form, the Organizing Secretariat will send a confirmation letter to each participant. Payment modalities All payments should be issued in EURO absolutely without bank charges. Payments can be made by: • Eurocheques or Taveller’s cheques payable to: M.A.F. Servizi s.r.l. -Torino (Italy) • Bank to bank transfer payable to MAF Servizi srl Torino, Cassa di Risparmio di Torino Ag. 5 – Torino – Italy, Account: C.C 1567585/65 ABI 6320 CAB 01005 Swift Code: CRTOITTT005 • Credit card payment (Visa or Master Card). Please specify the card number, owner, the participants name, expiration date, date of birth and signature on the registration form. Please mail all the registration documents together a copy of your payments to the Organizing Secretariat MAF Servizi. • To make the registration fast and match your own needs , the Organizing Secretariat strongly suggests to fill the forms for registration and hotel reservation request on the internet site at www.mafservizi.it /cytokine2002. Only registrations accompanied by payment will be accepted. Invoice The Organizing Secretariat will send the invoice referred to the payment of the registration fee. HOTEL ACCOMMODATION Hotel reservation Rooms in hotels of various price categories are available. All participants are requested to fill the hotel reservation form indicating only the chosen category. The accommodation will be allocated as availability at the moment of registration. A transfer service from and to the Congress Center at the beginning and at the end of the congress days will be provided for all the participants who have reserved the hotel through the Organizing Secretariat. Note To avoid any inconvenience, please make reservations as soon as possible. Hotel reservation Deadline: August 30 2002 After this date, the hotel accommodation cannot be assured. Upon receipt of the first night deposit plus Euro 14 as reservation fee, the Organizing Secretariat will send the room confirmation at latest 20 days before the Meeting. No reservation will be accepted without the payment of the first night deposit and 13
  • 14. reservation fee. Hotel rates indicate the price per room, per night, for bed and breakfast accommodation, taxes included. Cancellation of hotel reservation Written cancellations must be submitted to the Organizing Secretariat not later than September 7th 2001. In this case 70% of the reservation fee will be refunded; no cancellation request will be accepted after the above mentioned deadline. Confirmation Upon receipt of the payment of the first night deposit, the reservation fee and the completed registration form, the Organizing Secretariat will send a confirmation letter to each participant. Invoice The Hotel bill must be settled directly at the hotel, that will provide the participant with the relevant invoice, including the first night deposit. Check in and out times These are usually 2 p.m. and 11 a.m., respectively HOTELS RATES will be indicated on the Congress Website www.mafservizi.it/cytokine2002 xxxx HONORS AND AWARDS FOR THE ICS MEETING IN TORINO Awardees will be so identified in the meeting program. Kindly address queries and application forms (8 hard copies, no electronic submission) to Dr. Raymond Kaempfer, Chairman of Honors and Awards Committee, International Cytokine Society, Faculty of Medicine, The Hebrew University of Jerusalem, P. O. Box 12272, 91120 Jerusalem, Israel. Email: kaempfer@huji.ac.il; phone: 972-2-6758389; fax: 972-2-6784010. HONORARY LIFE MEMBERSHIP Nominations are solicited for Honorary Life Memberships in the International Cytokine Society. Each year, one individual will be awarded Life Membership as a tribute to his/her contributions to the field. Honorary Life Members are accorded all rights and privileges of active members, are exempted from Society dues and annual meeting registration fees, and are identified as Honorary Life Members in the Society Directory. Candidates will be elected by two-thirds majority vote of the Society Council, and will subsequently be informed in writing by the President. 14
  • 15. Nominations should be submitted to Dr. R. Kaempfer, at the above address no later than August 31, 2002. SHELDON WOLFF PRIZE IN CYTOKINE RESEARCH This Award ($1,000 and Meeting registration fee) was established by Dr. Charles A. Dinarello, in the name of the late Sheldon Wolff, M.D., of the New England Medical Center in Boston. This competition is open to any postdoctoral fellow (PhD or MD) and ICS member from an academic, non-profit institution. Whilst there is no age limit, the candidate is no longer eligible after 4 years of completed training. Candidates cannot be junior faculty at the time of abstract submission, and are not eligible if the research submitted was carried out other than in the mentor's laboratory. A statement from the candidate's scientific mentor testifying to the accuracy of these criteria must be provided. While candidates may apply each year, they are not eligible to receive the Award more than once. To enter this competition, candidates must submit an abstract and tick the appropriate box on the form. ED LEONARD PRIZE IN CHEMOTAXIS/CHEMOKINE RESEARCH This Award ($1,000 and Meeting registration fee) was established through grants from Novartis, Serono and Pfizer to honor Edward J. Leonard for his unique contribution to the field of leukocyte migration and chemokines. The prize will be given for experimental work on chemotaxis/chemokines by a full-time graduate or medical student or a postdoctoral fellow (MD or PhD) within 4 years of obtaining her/his degree who either is a member of the Society or is sponsored by an active member. The selections will be made by the Honors and Awards Committee on the basis of scientific merit, originality and presentation of scientific material. To enter this competition, candidates must submit an abstract, tick the appropriate box on the form and provide a letter from their Department Chairman certifying their student/postdoc status. ICS YOUNG INVESTIGATOR AWARD First, second and third prizes are $1,300, $1,100 and $900, respectively, in addition to Meeting registration fee. This competition is open to any investigator who is a member of the Society, or is sponsored by an active member. Applicants must have completed their postdoctoral training and currently hold a junior faculty position, or equivalent. The selection will be made by the Honors and Awards Committee on the basis of scientific merit, originality and presentation of scientific material. To enter this competition, candidates must submit an abstract and tick the appropriate box on the form. ICS POSTDOCTORAL INVESTIGATOR AWARD First, second and third prizes are $1,200, $1,000 and $800, respectively, in addition to Meeting registration fee. This competition is open to any 15
  • 16. postdoctoral fellow who is a member of the Society or is sponsored by an active member. Applicants must have completed their doctoral training and currently be engaged in full-time research. Persons who have completed a medical degree and are currently enrolled in a doctoral degree program are not eligible. The selections will be made by the Honors and Awards Committee on the basis of scientific merit, originality and presentation of scientific material. To enter this competition, candidates must submit an abstract and tick the appropriate box on the form. ICS OUTSTANDING SCHOLAR AWARD First, second and third prizes are $1,000, $900 and $800, respectively, in addition to Meeting registration fee. This competition is open to any full-time graduate or medical student who is a member of the Society, or is sponsored by an active member. The selections will be made by the Honors and Awards Committee on the basis of scientific merit, originality and presentation of scientific material. To enter this competition, candidates must submit an abstract, tick the appropriate box on the form and provide a letter from their Department Chairman certifying their student status. THE BOLTZMANN AWARD The Boltzmann Award, established by Austrian scientists, is meant to encourage international scientific cooperation in the field of cytokines. One award of $2,500 is granted to a pair of scientists from two countries selected jointly by the ICS and ISICR Awards Committees for an outstanding scientific presentation (oral, poster) at the biannual joint meeting of the two societies. Age of the authors nor membership in either society is a factor for selection. Work resulting from exchange programs (e.g., a postdoc in a foreign country publishing his findings with his host) will not be considered. To enter this competition, candidates must submit an abstract and tick the appropriate box on the form. THE FRIDERIKA FISCHER FOUNDATION FELLOWSHIPS The aim of these fellowships is to enable deserving young scientists from the former communist European countries to participate in annual ICS meetings. The number of fellowships will vary but no more than two per year will be awarded to applicants from any one country. A total of $10,000 is available for 2002, to cover travel of successful applicants to the meeting and help defray the cost of room and board. The registration fee will be waived for recipients. Applicants must (1) be permanent residents of one of the former communist countries in Europe (including all of Russia but excluding former East Germany), (2) have an abstract accepted for presentation and (3) be no more than 40 years old at time of application. Permanent residents of an eligible country who study or work temporarily abroad may also apply. Candidates must submit an abstract, tick the appropriate box on the form, and provide a brief CV with birth date and list of publications. Recipients will submit to the ICS Awards 16
  • 17. Committee a brief report on how meeting participation helped to advance professional goals. A copy of this report will be provided to The Friderika Fischer Foundation. 17