Past Recipients of The Howley Award
2011 Alisa Erika Koch, MD, Professor of Rheumatology at the University of Michigan and Andrew D. Luster, MD, PhD, Chief of Rheumatology, Allergy & Immunology and Director of the Research Center for Immunology & Inflammatory Diseases at Massachusetts General Hospital. Dr. Koch studied extensively at Northwestern and Loyola, concentrating on immunopatheogenesis, cell adhesion, angiogenesis and cytokines, as they relate to the treatment of rheumatoid arthritis (RA). Through her lab work and many contributions to prestigious scientific journals, Dr. Koch has made a major impact on RA treatments. Through his work at Duke, Rockefeller, Cornell and Harvard, Dr. Luster has been a pioneer in the birth, growth and development of the chemokine field. His laboratory at Massachusetts General Hospital has helped define how chemokines function in immune cell trafficking and in the patheogenesis of immune and inflammatory diseases like arthritis.
2010 Wayne M. Yokoyama, MD, of the Washington University School of Medicine in St. Louis. Dr. Yokoyama established the molecular basis of target cell recognition by natural killer cells. He was the first to identify a gene cluster encoding receptors responsible for inhibiting or activating natural killer cells, and to show that these receptors specifically interact with ligands that are expressed on the target cell surface.
2009 John O’Shea, MD, of the National Institutes of Health. Dr. O’Shea has elucidated the biochemical mechanisms of signal transduction in immunologic reactions and defined the molecular basis of immunodeficiencies. He has identified key biochemical steps by which cytokines exert their effects in immunologic and rheumatic diseases and these findings have in turn led to the development of a new class of immunosuppressive drugs.
2008 Gerard Karsenty, MD, PhD, of Columbia University College of Physicians. His contributions to our understanding of the development and function of the skeletal system have been nothing short of remarkable. To put it succinctly, Karsenty has singlehandedly transformed this field. Prior to Karsenty’s work, little was known about the molecular basis of mammalian skeletal system development and differentiation. Now, a decade later, the field is burgeoning with a plethora of new transcription factors, coactivators, corepressors, and signaling pathways that explain the development of the osteoblast from the mesenchymal stem cell, both during embryonic development and during postnatal bone formation. Michel Nussenzweig, MD, PhD, of Rockefeller University. Dr. Nussenzweig’s contributions to the fields of B cell development and dendritic cell function have provided important insights into the etiology of autoimmune diseases such as rheumatoid arthritis and have paved the way to the development of novel therapies for the treatment of these diseases.
2007 David Wofsy, MD, of the University of California at San Francisco, for initiating the use of so called biologic agents for the treatment of rheumatic disease and for establishing a large clinical trial network for evaluating the use of these agents in humans with lupus. His more recent studies led to the development of clinical applications of a new biological agent that inhibits T cells. One such medication known as aratacept is now in use for the treatment of rheumatoid arthritis. Gary Koretzky, MD, PhD, of the University of Pennsylvania, for his studies of the molecules that white blood cells use to control their function. One of these molecules is known as SLP-76. Koretzky’s studies demonstrated how signals delivered by extra-cellular molecules such as antigens can be linked to the control of protein molecules inside cells.
2006 Gary Firestein, MD, of the University of California, San Diego. His scientific contributions have moved the study of RA from primitive analysis of peripheral blood cells to a sophisticated assay of patterns of gene expression which provide a much more powerful and informed perspective.
2005 Chella David, PhD, of the Mayo Clinic, for his studies, first on genetic fine structure controlling susceptibility to collagen-induced arthritis and then on the functional HLA Class II Transgenic Mice, which enabled his laboratory and those of others to study human disease with humanized models.
2004 David Felson, MD, MPH, of Boston University, for his contributions in the fields of clinical epidemiology and clinical trials design, and Jeffrey Ravetch, MD, of Rockefeller University, for his contributions toward understanding the role of Fc receptors, immune mediated inflammation and the implications for therapeutic interventions
2003 David V. Goeddel, PhD, of Tularik Inc., in recognition of his important contributions to the biology of TNF, which were pivotal in the development of TNF inhibitors.
2002 Betty Diamond, MD, of Albert Einstein College of Medicine, for her work to elucidate the cause of lupus and to understand how the various forms of tissue injury are induced in patients with this disorder. Peter Lipsky, MD, of the National Institutes of Health. Taking a leadership role in the development of new biologic agents for the treatment of RA, Dr. Lipsky played a key role in investigations of anti-TNF or infliximab.
2001 David S. Pisetsky, MD, PhD, of Duke University, for his work on the immune properties of DNA. This work in the area of SLE has revolutionized the conceptualization of the role of DNA in normal and aberrant immunity and has provided a new paradigm of autoimmunity.
2000 Daniel Kastner, MD, PhD, of the National Institutes of Health, for his work on genetic mapping and positional cloning. He successfully organized and led an international consortium of groups that were in search of the gene for familial Mediterranean fever, a form of arthritis particularly common in Mediterranean populations.
1999 Morris Reichlin, MD, Oklahoma Medical Research Foundation, for his work to determine the role of specific immunological factors in the pathogenesis of SLE. His most recent work on the anti-P system is potentially important in terms of access of circulating antibodies to internal cellular compartments and their ability to cause disease.
1998 Matthew H. Liang, MD, MPH, of the Brigham & Women’s Hospital, for his studies of the social and economic consequences of arthritis, the roles of medical, surgical and physical therapy on long term outcome of these diseases and how patients and their families learn coping skills; and William P. Arend, MD, of the University of Colorado, for his pioneering research, which has provided an increased understanding of natural mechanisms to counter inflammation, and has led to entirely new approaches to the treatment of many types of arthritis.
1997 Arthur Weiss, MD, PhD, University of California, San Francisco, discovered key elements that activate white blood cells, called T cells, in the inflamed tissues in joints of patients with rheumatoid arthritis.
1996 Michael B. Brenner, MD, Brigham and Women’s Hospital, for his seminal discoveries of how lymphocytes recognize foreign molecules that can serve as triggers for various forms of arthritis and other inflammatory diseases, and Laurie H. Glimcher, MD, Harvard School of Public Health, for her pioneering work on deciphering the molecular controls that determine the chemicals, termed cytokines, that lymphocytes produce in fighting infections and in causing inflammation in arthritis.
1995 Barton F. Haynes, MD, Duke University, for his work on understanding the role of retroviruses and biologically active molecules in the pathogenesis of inflammatory synovitis.
1994 K. Frank Austen, MD, Harvard Medical School, for his outstanding contributions to understanding of the molecular and cellular biology of the inflammatory system, which is involved in many types of arthritis. Dr. Austen has been instrumental in identification of a number of chemicals called leukotrienes, which are involved, in the inflammatory response.
1993 Allen C. Steere, MD, New England Medical Center. Dr. Steere and his colleagues discov¬ered Lyme disease, described its numerous clinical manifestations, and helped forge a link between the disease and the tick-borne microorganism, Borrelia burgdorferi.
1992 Darwin J. Prockop, MD, PhD, Thomas Jefferson Medical College, for his pivotal findings on how collagen is made. They are the basis for his hypothesis that the premature degeneration of collagen tissue in man can be the result of genetic defects in the collagen molecule itself.
1991 John P. Atkinson, MD, Washington University School of Medicine, and Douglas T. Fearon, MD, Johns Hopkins University, used the latest techniques in molecular biology to isolate the genes that make both complement proteins and the cell proteins that interact with complement.
1990 Robert J. Winchester, MD, Columbia University, for his pioneering research that identified the basis for a person's genetic predisposition to develop rheumatoid arthritis.
1989 Eng M. Tan, MD, Scripps Clinic and Research Foundation, for his lifelong study to identify autoantibodies in those arthritis diseases falling into the category of autoimmunity, including systemic lupus erythematosus, scleroderma, and Sjögren's syndrome.
1988 Mart Mannik, MD, University of Washington, for his contributions to understanding of rheumatoid arthritis, especially to understanding the structure of antibody molecules, including the unique characteristics of antibody idiotypes.
1987 Dennis A. Carson, MD, Scripps Clinic, for his work in purine metabolism in the immune system and the nature of idiotypic specificities in rheumatoid factors.
1986 Hugh O. McDevitt, MD, Stanford University, for his contributions to the understanding of cellular and molecular mechanisms involved in the genetic control of immune responsive¬ness.
1985 C. William Castor, MD, University of Michigan, for his work in the definition, function and biological significance of connective tissue activation and the connective tissue activating peptides.
1984 Joan A. Steitz, PhD, Michael Lerner, MD, PhD, and John A. Hardin, MD, Yale University, for their work in the identification of prominent autoantigens in systemic lupus erythematosus.