Alan G Baxter Ph.D., M.B., B.S.
Molecular Sciences Bldg 21, James Cook University,
Townsville, 4811, Queensland, Australia
Telephone: 61-7-4781 6265 Fax: 61-7-4781 6078
Baxter is a medical graduate who completed a PhD in immunogenetics at the Walter and Eliza Hall Institute under the supervision of Tom Mandel. He has worked as a Research Fellow at Harvard Medical School and at Cambridge University, where he was a Supervisor in Pathology for Trinity College. He is known internationally for his contributions to the genetics of autoimmune disease and has published pioneering work on the genetics of gastritis and the role of NKT cells in autoimmunity, and made major contributions to our understanding of gene/environment interactions in autoimmune disease. He has been a member of the Australasian Society for Immunology since 1994 and was President of the Society from 2006-2008, and is currently on an NHMRC Grant Review Panel, a New Zealand Health Research Council review panel, and the MSRA Research Management Council. He is a member of the editorial boards of Immunology and Cell Biology and The Review of Diabetic Studies and is a reviewer for several journals including Nature Medicine, Science, The Lancet, Diabetologia, Autoimmunity, and the Journal of Immunology. His extensive commitments to the public appreciation of science have helped promote rational discussion of the health sciences in Australia. He established the Autoimmunity Research Group at the Centenary Institute, where he worked for nine years before taking up his current appointment as Professor of Biochemistry and Molecular Cell Biology at the Comparative Genomics Centre of the James Cook University. His work is funded by the NHMRC, ARC and Lions Clubs. Baxter is currently Head of the Comparative Genomics Centre at James Cook University.
Significant scientific achievements include:Baxter studies gene/environment interactions in immune regulation and autoimmunity; particularly novel is his emphasis on innate immunity. As one of the pioneers in the NKT cell field, he was the first to demonstrate their effects in autoimmunity (J Exp Med 187:1047; cited over 500 times) and his lab leads the world in the genetic control of NKT cell development and function, having recently shown normalisation of NKT cell numbers by transgenic complementation of Slamf1 (J Immunol. 186:3953). His studies on the role of bacteria in autoimmunity included the development of the NOD mouse strain as a model of mycobacteria-induced lupus (Immunol 83:227), have resulted in a patent for the use of MAPG to prevent Type 1 Diabetes (T1D), and also caused the withdrawal of several BCG vaccine strains and a vaccine platform (transcutaneous immunisation) following the demonstration that they induced T1D and Experimental Autoimmune Encephalomyelitis, a mouse model of Multiple Sclerosis (MS). This focus has most recently dissected the role of Toll-like Receptors in EAE, producing for the first time a molecular mechanism for the effects of bacteria on autoimmunity (J Immunol. 187:791).