George Mackaness, who coined the term, “activated macrophage”, to describe the enhanced antimicrobial function acquired by macrophages in response to infection with intracellular, bacterial pathogens, died on March 4, at age 83, in Charleston, SC, after a long bout with Alzheimer's disease. He is survived by his son, Miles, and three grandchildren. George was born in Sydney, Australia. He obtained his M.D. and B.S. degrees from the University of Sydney in 1945, did his residency at Sydney Hospital, and traveled to England in 1947 to obtain a Diploma in Clinical Pathology from the British Postgraduate School of Medicine at London University. He earned his Ph.D. degree at the William Dunn School of Pathology, University of Oxford, under the mentorship of Nobel Laureate, Sir Howard Florey, with whom he continued to work as a Senior Fellow. In 1954 he moved to Canberra, Australia, to set up the Department of Experimental Pathology in the John Curtain School of Medical Research at the Australian National University. He later moved to South Australia to accept the position of Professor of Microbiology at the University of Adelaide. In 1965 he was appointed Director of the Trudeau Institute in Saranac Lake, New York, a position he held before becoming President of the Squibb Institute for Medical Research in Princeton, New Jersey, in 1976. He retired to the Charleston area in 1987. During his time at Oxford George studied the action of antituberculous drugs on the tubercle bacillus inside macrophages, an experience that made him aware of the difficulty of working with this slow growing pathogen and the need to find another facultative intracellular bacterium with which to investigate cellular immunity to infection. It was during his time at the John Curtin School that he chose to work with Listeria monocytogenes . His studies in the 1960s showed that although immunity to listeriosis in mice is mediated by “specifically-sensitized” lymphocytes, it is expressed nonspecifically by macrophages with enhanced microbicidal function. He went on to show, among other things, that the transfer of lymphocytes from Listeria -infected donor mice to recipient mice caused the recipients to quickly acquire a high level of immunity that was associated with activation of their macrophages to an enhanced microbicidal state. It was later shown that Listeria -specific lymphocytes activate macrophages by way of secretion of soluble factors now known as lymphokines. Many of the findings generated with the Listeria model apply to intracellular pathogens in general, including Mycobacterium tuberculosis . The model continues to generate important information in many laboratories throughout the world. George was awarded the Paul Ehrlich-Ludwig Darmstaedter Prize for Medicine in 1975 and the Norvartis Prize for Clinical Immunology in 1998. He was elected to the Royal Society in 1976. He remained modest and of pleasant temperament throughout his career. I joined his laboratory at Trudeau Institute as a postdoctoral fellow in 1967 and remained in contact with him until his retirement. He was an excellent mentor. Those of us who worked with him are deeply saddened by his death.</P>
Tuberculosis – Elsevier
Published: Jul 1, 2007
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