Informing the development of the next-generation malaria vaccines by:
- identifying and characterising key functional mechanisms of antibodies that mediate protection,
- defining the key cellular mechanisms that promote the generation of functional antibodies, and
- quantifying the impact of host age and prior malaria exposure on antibody development.
Dr Michelle Boyle completed her PhD in 2012 at the Burnet Institute and Melbourne University with a focus on developing methods to study Plasmodium falciparum malaria invasion of red blood cells and progressing towards vaccine and drug development.
Following her PhD, Michelle was awarded an NHMRC Early Career (CJ Martin) Fellowship and completed a two-year post-doctoral position at the University of California, San Francisco. Her work identified a number of age and malaria exposure-dependent changes to T cells that contribute to naturally acquired immunity and she received the Australian National Association of Research Fellows Postdoctoral Investigator Award in 2015.
Dr Boyle was working on collaborative projects between the Menzies School of Health Research in Darwin, where she is an Honorary Fellow, and the Burnet Institute, to identify mechanisms contributing to the acquisition of immunity against multiple malaria species in the South East Asia region.
In 2018, she established her lab at the QIMR Berghofer Medical Research Institute in Queensland and commenced as an EMBL Australia Group Leader. In 2022, Dr Boyle was awarded a prestigious CSL Centenary Fellowship that will see $1.25 million over five years go towards her cutting-edge work boosting protection against malaria. In early 2023, Dr Boyle relocated to the Burnet Institute in Melbourne and remains an honorary group leader at QIMR Berghofer.
Science Advances (2019) 5(9).
|IgM in human immunity to Plasmodium falciparum malaria.
Science Translational Medicine (2019) 11 (474).
|Challenges and strategies for developing highly efficacious and long-lasting malaria vaccines.
JCI Insight (2018) Nov 15;3(22).
|Loss of complement regulatory proteins on uninfected but not infected red blood cells in P. vivax andP. falciparum malaria.
Immunity (2015) 42:580–590.
|Human antibodies fix complement to inhibit Plasmodium falciparum invasion of erythrocytes and are associated with protection against clinical malaria.
Journal of Infectious Disease (2015) 212:416-425.
|The effector phenotype of Plasmodium falciparum-specific CD4 T cells is influenced by both age and transmission intensity in naturally exposed populations