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.
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.
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
(firstname.lastname@example.org), 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.
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
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,
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.
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
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
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
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
Byron H. Waksman, 9/4/2001
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
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
PG: Charles, exactly how many patients receiving anti-TNF therapies have experienced a
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
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
PG: What have the regulatory agencies done to advise physicians on the risks of chronic
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
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
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.
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-
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
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.
Newsletter of the International Cytokine society
International Cytokine Society
Biotech Park, Suite 9, 1021 15th street, Augusta, GA 30901
Telephone: (706) 722-7511; Fax: (706) 722-7515
President: Nancy Ruddle
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Junior Councilor: Mathew Fenton
Past President: Jean-Michel Dayer
Treasurer: John Hiscott
Secretary: Ann Richmond
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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: email@example.com
Opinions expressed by contributors are not necessarily those of the International Cytokine
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:
Josef D. Schwarzmeier
International Advisory National Advisory
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)
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)
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Participants are invited to submit abstracts of their work for oral or poster
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Abstracts will be only accepted if sent together with the registration fee within the
deadline of 15 June, 2002.
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Oral presentation of selected papers (see detailed programme on Workshops)
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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
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
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.
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
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: firstname.lastname@example.org; phone: 972-2-6758389;
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.
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
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
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
Committee a brief report on how meeting participation helped to advance
professional goals. A copy of this report will be provided to The Friderika