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Editor-in-Chief
It has been eight years since the Society of Leukocyte Biology councilors initiated cash awards in honor of Dolph Adams. The $1000 award was established to recognize the most highly cited research paper and review article published in the Journal of Leukocyte Biology (JLB). The award is based on the number of citations over the past 5 years as a measure of the impact of the papers. The prizes are awarded to the corresponding authors who decide how to share it with their coauthors. The 2004 Dolph Adams Award winner who had the highest number of citations from 1999 through 2003 in the review category with 173 citations was coauthored by Cees van Kooten and Jacques Banchereau and was entitled, "CD40-CD40 ligand" (J. Leukoc. Biol. 67, 2–17, 2000). The most highly cited award-winning research article with 91 citations was by Hong-Bing Shu, Wen-Hui Hu, and Holly Johnson, entitled "TALL-1 is a novel member of the TNF family that is down-regulated by mitogens" (J. Leukoc. Biol. 65, 680–683, 1999).
It is one of the highlights of my role as Editor-in-Chief of JLB to notify authors that they have won the Dolph Adams Award. For 2005, the most highly cited research article with 100 citations was by Bryan W. Jones, Terry K. Means, Kurt A. Heldwein, Marc A. Keen, Preston J. Hill, John T. Belisle, and Matthew J. Fenton, entitled "Different Toll-like receptor agonists induce distinct macrophage responses" (J. Leukoc. Biol. 69, 1036–1044, 2001). The authors are usually very pleased to hear such good news. For Matthew Fenton, the news provided additional recognition of his successful research career, in particular, as he recently left his laboratory and position as professor of Medicine, Immunology and Microbiology at the University of Maryland Medical School to become chief of the Asthma, Allergy and Inflammation Branch in the Extramural Division of National Institute of Allergy and Infectious Diseases, National Institutes of Health (NIH). However, as he is now in an executive managerial position with the federal government, rigorous ethical requirements were applicable, and he needed permission from a NIH conflict-of-interest committee to accept this award. I had to document that the award was longstanding and bonafide, that it was sponsored by a society of scientists independent of biotechnology and pharmaceutical interests, that the funds for the award came collectively from the scientific members of the society, and that it was democratically awarded based on objective criteria. Could there have been a concern that undue influence exerted by this award might alter the course of federal research policy and administration? Fortunately, the committee approved Dr. Fenton’s award, and he is now free to split it amongst all seven coauthors.
It is to Dr. Fenton and his colleagues’ credit that their paper was actually based on a rational hypothesis. They proposed in 1999 that as the sequence of the intracellular signaling domains for Toll-like receptor 2 (TLR2) and TLR4 was somewhat different, this could actually result in the activation of different signal transduction pathways and gene targets; and TLR4-mediated activation of nuclear factor (NF)-
B still occurred in knockout mice lacking the adaptor protein MyD88, whereas TLR2 engagement failed to activate NF-B, thus indicating that the signal transduction pathways used by these to TLR proteins were not identical. They subsequently compared the responses of cultured macrophages stimulated by Mycobacterium tuberculosis (Mtb) culture filtrates. They observed that the resultant culture filtrates activated cells via TLR2 and tentatively identified the responsible components of Mtb as the glycolipids lipoarabinomannan and phosphatidylinositol dimannoside. This represented the first identification of glycolipid ligands for TLR2. These glycolipid TLR2 ligands and the TLR4 ligand Escherichia coli lipopolysaccharide induced the secretion of tumor necrosis factor by macrophages. In contrast, only TLR4 engagement resulted in the production of nitric oxide. This highly cited, pioneering study stimulated considerable research, resulting in the mapping of differences in signaling by the various TLRs over the following 4 years.
The other coauthors have since pursued various careers. Bryan Jones has evolved from being a lab technician to being a law student with an interest in biotechnology. Terry Means, who was a graduate student in 2001, is now an instructor at Harvard’s Massachusetts General Hospital. Kurt Heldwein, who was a postdoctoral fellow in 2001, is now a staff scientist at the Novartis Institutes for Biomedical Research. Preston Hill is a research associate in the Department of Microbiology, Immunology, and Pathology at Colorado State University, where Dr. John Belisle holds the position of associate professor. Marc Keen is currently a research technologist at the University of Nebraska Medical Center. It is evident from the above that life goes on but that authors of award-winning papers use their research experience in their subsequent careers.
We also recognize and honor the five runner-up research articles with 90–51 citations, respectively, as follows:
Dr. Robert Strieter recalls that I invited him to contribute a review about the role of CXC chemokines in angiogenesis after I heard his presentation at a Keystone Conference on chemokines in 1999. This review is the Dolph Adams award-winning article with 176 citations for 2005. The authors were John A. Belperio, Michael P. Keane, Douglas A. Arenberg, Christina L. Addison, Jan E. Ehlert, Marie D. Burdick, and Robert M. Strieter, and it is entitled, "CXC chemokines in angiogenesis" (J. Leukoc. Biol. 68, 1–8, 2000).
This review of the role of CXC chemokines in angiogenesis was completed prior to Dr. Strieter’s move from the University of Michigan to the University of California Los Angeles (UCLA) in January 2000. The review was based on a series of studies from his lab and others that began in 1989 with the initial observation that interleukin (IL)-8 was expressed in the tissues of various disease states (i.e., cancer, pannus of rheumatoid arthritis, and pulmonary fibrosis) and was not always associated with an infiltration of neutrophils. In fact, the localization of IL-8 in these tissue specimens was often highly associated with areas of angiogenesis. On this basis, it was hypothesized that IL-8 was a potent angiogenic factor. Subsequent identification and characterization of IL-8 as a potent angiogenic factor was published in Science in 1992. The concept of IL-8 as a member of the CXC chemokine family and an angiogenic factor was extended to include all members of the CXC chemokine family, which contained the conserved motif of glutamic acid-leucine-arginine (ELR+). In 1995, it was determined on a structural/functional level that all ELR+ CXC chemokines were found to be potent proangiogenic factors, whereas interferon (IFN)-inducible CXC chemokines, which lacked the conserved ELR motif, were potent inhibitors of angiogenesis. For example, if the ELR motif in IL-8 were mutated to the DLQ or TVR sequence present in non-ELR+ CXC chemokines [i.e., platelet factor 4 and IFN-inducible protein 10 (IP-10), respectively], the mutant IL-8 was converted to an inhibitor of angiogenesis. This work subsequently led to studies to determine whether CXC chemokines were important in the regulation of angiogenesis related to diseases, which were associated with aberrant angiogenesis. Dr. Strieter’s laboratory showed that two ELR+ CXC chemokines, IL-8 and epithelial-derived neutrophil-activating factor-78, were important in promoting angiogenesis in non-small cell lung cancer (NSCLC). Conversely, IP-10 or monokine induced by IFN-
non-ELR+CXC– chemokines were potent angiostatic factors that attenuated NSCLC tumor growth by inhibiting tumor-associated angiogenesis. This work ultimately resulted in the discovery that CXC chemokine receptor 2 (CXCR2) is the putative receptor that mediates the angiogenic effects of ELR+ CXC chemokines. Recently, another Dolph Adams award-winning laboratory headed by Dr. Romagnani has shown that the expression of CXCR3B on endothelium is the receptor for mediating the angiostatic effects of non-ELR+ CXC chemokines. Dr. Strieter is continuing his efforts to show the pivotal importance of ELR+ CXC chemokines as angiogenic stimulants in pulmonary fibrosis, cancer, and other disorders. He is investigating the inter-relationships of angiogenic and angiostatic CXC chemokines with other angiogenic factors. He supports the notion that optimal inhibition of angiogenesis will require targeting of more than one factor to reduce tumor growth more effectively.
Dr. Strieter is currently the professor and chief of the Division of Pulmonary and Critical Care Medicine and vice-chair of the Department of Medicine. A number of his coauthors moved with him to UCLA as follows: Dr. John Belperio is now an assistant professor, and Dr. Michael Keane is an associate professor at UCLA; Ms. Marie Burdick is still his chief technician. Dr. Douglas Arenberg is an associate professor at the University of Michigan, Dr. Christina Addison moved to the Center for Cancer Therapeutics in Ottawa, Canada, and Dr. Jan Ehlert is currently at the Tumor Biology Center in Freiberg, Germany. Overall, Dr. Robert Strieter and his colleagues represent a shining example of scientists–clinicians who are effectively engaged in translating fundamental laboratory findings to the bedside.
We also recognize and honor the five runner-up review articles with 137–64 citations, respectively, as follows:
JLB continues to be in excellent fiscal health based on page charges, advertising revenue, and institutional subscriptions. Fortunately, this enables us to cover the expenses of publishing articles online within 1–3 weeks of acceptance as "JLB preprints." Our online submission and review systems have enabled us to manage the increased number of submitted papers which is headed for the 700–800 range this year. The online processing also enables us to provide an initial review of papers by 1 month on the average while re-reviews take an average of 25 days. The quality of the papers submitted to JLB has also improved our acceptance rate which is at 38%. Despite increasing competition from commercial publishers, our citation index impact factor is stable at 4.22 as compared with 4.18 in 2004. JLB ranks 10th of the 62 hematology journals and 10th of the 100 or so peer-reviewed immunology articles. We evidently fulfill a need for articles focused on the cell biology of host defense for the scientific community. We are continuing to invite overviews from plenary speakers and papers from participants at selected meetings. The overview contributions are cited twice as often as the unsolicited papers; reviews, three times as often.
JLB has initiated inclusion of a new category of brief reviews entitled Conceptual Perspectives. A number of them have already been published. They are intended to provide authors with the opportunity to express their opinions about controversial issues. Too often nowadays. authors can not clearly espouse their hypotheses in papers, and they are frequently overwhelmed by factual details in authoritative reviews. The Conceptual Perspective articles aim to emphasize ideas with only limited documentation of the facts, including only one table or figure and a few references. It has, however, been difficult to solicit such articles. Investigators are understandably reluctant to publicize their ideas before they have the data in press. We would appreciate your suggestions for potential contributors with good ideas.
Long-term, we are concerned about how long we should continue to produce a print version of JLB as more and more scientists become dependent on the internet as their source of research information. Conversion to an online journal reduces journal production costs only by about 25%. Consequently, the cost of journal production will have to shift from the scientific consumers to the contributors of the papers. We appreciate your suggestions and ideas for further improvement of JLB.
Received August 25, 2005; accepted August 26, 2005.
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