Associate Professor Michelle Wykes and her Molecular Immunology Group studies the immunology behind several diseases. Their research initially focussed on understanding the role dendritic cells play in the pathogenesis of malaria and now apply novel insight gained into understanding cancer and inflammatory bowel disease. They have found novel functions for Programmed cell death-1 ligand 2 (expressed on dendritic cells) in regulating immunity. More recently, their focus has shifted to developing novel immunotherapies.
Current QIMR Berghofer appointment
- 2017 – present: Group Leader, Molecular Immunology
- 2012 – 2017: QIMR Berghofer Team head
- 2013 – 2016: ARC Future Fellow
- 2012 – 2013: Senior Lecturer, School of Medicine, The University of Queensland.
- 2010 – 2012: Smart Future Fellow (Senior Level), QIMR.
- 2008 – 2010: Assistant Lab Head, QIMR.
- 2001 – 2008: Senior Research Officer, QIMR.
- 1999 – 2000: Team Leader: Cellular Interaction Team, Brisbane, Mater Medical Research Institute.
- 1996 – 1999: Sir William Dunn School of Pathology, University of Oxford.
- 1993 – 1996: Department of Immunology, Royal Postgraduate Medical School.
Current Area of Research
- Investigating the role of checkpoint inhibitors in the pathogenesis of malaria and the role of dendritic cells in the chronicity of malaria
- Identified that dendritic cells, which are the sentinel of immunity, take up proteins (pathogens), package them into vesicles of native proteins, and transfer these proteins to naïve B cells to initiate antibody responses and isotype switching of B cells.
- Identified that dendritic cells had a role in initiating immunological tolerance.
- Showed dendritic cells and follicular dendritic cells express a novel ligand for CD38 which mediate their maturation and expansion respectively, and signaling this ligand in vivo, with soluble CD38 can more than double the life span of immunological B cell memory.
- Identified expression of CD154 on B cells. This study explained gaps in our understanding of B cell activation.
- Showed that long term protection by memory B cells and long lived plasma cells specific for the malaria vaccine underwent apoptosis following infection. This finding would explain why >40 clinical trials for various malaria vaccines, which were based on B cell-mediated protection, would have failed in the field.
- The strain of Plasmodium causing malaria determines the capacity of dendritic cells to initiate immune responses resulting in a dichotomy of the phenotype and function of dendritic cells between lethal and non-lethal malaria.
- Plasmacytoid dendritic cells (PDC) are a novel cell for Plasmodium survival and replication which provides a niche to escape immune–surveillance and permit chronicity of the disease. This is the first major advance on our understanding of the blood-stage Plasmodium life cycle since the 1950s.
- Identified CD8 T cells are required for sterile immunity against malaria but Programmed cell death-1 mediates a loss of these cells leading to chronic or recrudescent malaria.
- Identified CD8 T cells are required for long term protection against malaria but Programmed cell death-1 mediates a loss of these cells.
- Programmed cell death-1 Ligand 2 (PD-L2) has a regulatory role in mediating immunity.
- 1990 – current: Australian Society of Immunology
- 2010 – current: Australian Society of Parasitology
- 2007: 2006 Ross Hohnen Award for research excellence. Award for best research proposal “Evaluation of the protective potential of J8-specific T and B cells in protection against S. pyogenes infection.”
- 2009: Griffith University Encouragement Award
- 2010: Smart Future Fellowship, Queensland State Government
- 2013: Future Fellowship, Australian Research Council
- 2015: Kavli Frontiers of Science Fellow, USA National Academy of Science
- 1993: Doctor of Philosophy, University of Western Australia
- 1986: Bachelor of Science (Hons), University of Western Australia