Garvan welcomes Professor Chris Goodnow as Deputy Director
Professor Chris Goodnow
Media Release: 01 February 2015
The Garvan Institute of Medical Research is delighted to announce that distinguished immunologist and molecular geneticist, Professor Chris Goodnow FAA FRS, has now taken up his position as the Institute’s Deputy Director.
Professor Goodnow has also assumed The Bill and Patricia Ritchie Foundation Chair, and is setting up a lab in Immunogenomics to investigate the underlying genetic causes of immune disorders, particularly autoimmune diseases (which attack the ‘self’).
Goodnow is current President of the Australasian Society for Immunology. His research has been recognised by a number of awards and honour, including: American Association of Immunologists (AAI) Pharmingen Investigator Award; AAI Distinguished Lecturer; Australasian Society for Immunology Burnet Orator; Gottschalk Medal; Health Minister’s Prize; Centenary Medal; Ramaciotti Medal; GSK Award for Research Excellence; Fellowship of the Australian Academy of Science; Fellowship of the Royal Society; and Membership of the US National Academy of Sciences.
Immediately prior to joining Garvan, Goodnow led the Division of Immunology at the John Curtin School of Medical Research, Australian National University (ANU). He joined ANU in 1997 as Professor and Director of the Medical Genome Centre, leading its development into a Major National Research Facility, the Australian Phenomics Facility.
With an American father and Australian mother, Goodnow grew up in Washington DC before moving to Sydney as a teenager. He trained in veterinary medicine and surgery, immunochemistry, and immunology at the University of Sydney, and in molecular biology at Stanford University, California. After doctoral studies at Melbourne’s Walter and Eliza Hall Institute of Medical Research and the University of Sydney, he joined the faculty of Stanford University Medical School and the Howard Hughes Medical Institute in 1990.
Throughout his career, Goodnow has been fascinated by how the immune system makes its decisions, in particular how it distinguishes between ‘self’ and ‘non-self’. Immune cells must decide very quickly whether they are looking at an invading microbe, which poses a threat, or a part of the body, which should be protected.
Everything in the immune system goes into making that decision as accurately as possible, because getting it wrong can lead to devastating consequences, including autoimmune diseases like type 1 diabetes, rheumatoid arthritis, multiple sclerosis and Sjögren's syndrome.
“Teasing apart the critical decision the immune system must make has taken me on an Odyssey,” said Goodnow.
The first phase of that Odyssey, during his PhD, involved the creation of genetically engineered mice to track exactly what happened to individual antibody-producing cells (B cells) in mice when those cells first encounter ‘self-antigen’ – their own bodies – or ‘foreign antigen’.
Then, at Stanford University, Goodnow created many different mice with very specific mutations in both B cells and T cells, the killer cells of the immune system. This allowed him to track exactly what happened, at a molecular level, when immune cells made decisions, in tandem, about what to destroy and what to protect.
“One thing I demonstrated fairly early in my career was that the immune system imposes a whole series of checkpoints on cells as they develop – much like the checkpoints during an intercontinental ballistic missile launch,” he said.
Much of Goodnow’s work at Stanford involved introducing known genetic mutations associated with autoimmune diseases into mice with very well defined B and T cells.
“That way, we could monitor all the cellular events, including which checkpoint was disrupted and how. It was very productive, but we quickly exhausted the world’s supply of spontaneous mouse mutants that had autoimmune diseases due to single gene defects.”
So Goodnow addressed his supply problem by returning to Australia and establishing a very large and sophisticated mouse breeding facility in Canberra, where he could introduce new mutations.
For much of the last 18 years, Goodnow has taken mice with abnormal immune systems – autoimmune diseases, or immune deficiencies, or cellular abnormalities in the blood – and then analysed their genes.
Latterly, he has worked the other way around, first understanding the genetics, and then observing whether or not the mice had a genetic abnormality.
This was how one of his heroes, Nobel laureate Sydney Brenner, predicted almost 20 ago that analysis of the immune system would have to be done – once sequencing became affordable.
While at Garvan, Goodnow will take full advantage of the powerful whole genome sequencers in Garvan's Kinghorn Centre for Clinical Genomics, as well as in-house capacity to engineer mice with highly specific genetic mutations.
At the same time, he hopes to establish a network of people working in the field of autoimmunity in order to pinpoint the origin of disease – and then to fix it. “There is a terrific network of clinical immunologists, endocrinologists, oncologists and paediatricians in various hospitals around Sydney,” he said.
“I’m hoping that we can complement that clinical expertise with our findings from the genomic and molecular immunology end.”
Garvan immunologist Emeritus Professor Tony Basten FAA FTSE, who was department head at the University of Sydney when Goodnow did his PhD, says that Garvan is fortunate to attract Goodnow.
“It was evident even when Chris was a PhD student, that he had a unique ability to sense where immunology was going,” said Professor Basten.
“As a result of Chris’s initiative we were the first Australian lab to apply transgenic technology to studying the immune system.
“He’s a brilliant scientific strategist, which means that he’s always two years ahead of the field.”
Executive Director of Garvan, Professor John Mattick AO FAA FRCPA, is very pleased about the arrival of his new Deputy. "Professor Goodnow is one of Australia’s most outstanding scientists, who will greatly strengthen Garvan’s preeminence in human genomics,” he said.