WEHI Immunity Special Seminar hosted by Dr Rhea Longley

Associate Professor Michelle Boyle 

Working Group Head

Cellular Responses to Disease and Vaccination

Snow Fellow, CSL Centenary Fellow, EMBL Australia Group Leader

Burnet Institute

Germinal centre responses in human malaria infection 

Davis Auditorium

Join via TEAMS

Including Q&A session

Associate Professor Michelle Boyle is a Snow Medical Fellow, CSL Centenary Fellow, and Head of the Cellular Responses to Disease and Vaccination working group. Michelle completed her PhD in at the University of Melbourne in 2012, focusing on antibody response that protect from malaria. From 2013 to 2015, she was an NHMRC CJ Martin Early Career Fellow at University of California, San Francisco. Returning to Australia, Michelle developed an independent program focused on cellular mechanisms driving human immunity to malaria. In 2018, she was recruited as a Team Head to QIMR‐Berghofer and moved her program to Burnet Institute in 2023. 

Michelle’s research aims to develop vaccines and therapeutics for malaria through novel insights in human immunity. She has made fundamental discoveries of specific types and functions of antibodies that protect from malaria, and the CD4 T cells that drive protective responses, along with the mechanisms of anti-disease regulatory networks that prevent immunopathology during infection. To translate her findings, A/Prof Boyle has led a human malaria infection clinical trial to investigate if host directed therapy can boost immune development. Her Snow Fellow funded program focuses on investigating immunity directly within secondary lymphoid tissues in human infection. 

Clinical immunity to malaria develops rapidly, with one or two infections inducing coordinated regulatory anti-disease responses that protect from immunopathology by restraining inflammation. While essential for preventing severe disease, these regulatory responses come at a cost: the same anti-disease mechanisms hamper parasite-clearance and antibody development including those induced by vaccines. Understanding the underlying mechanisms of regulatory and effector responses is essential for developing approaches that may boost vaccine immunogenicity and efficacy in exposed populations. 

Antibody development in response to infection and vaccination occurs within secondary lymphoid tissues, where antibody secreting plasma cells and memory B cells develop with support of CD4 T follicular helper cells. Studies of these processes in human infection are severely limited due to constraints accessing secondary lymphoid tissues. To overcome this challenge, we have developed critical cohorts of secondary lymphoid tissues from malaria exposed and infected donors (spleens and tonsils).  Multi-omic analysis of tissue samples has identified parasite species specific regulatory programs including expanded Type I regulatory CD4 T cells in P. falciparum and activated CD8 T cells in P. vivax infection. To model specific responses to parasites and vaccines, we have optimized in vitro human lymphoid culture models to complement ex vivo analysis. This model recapitulates important characteristics of the immune response to malaria, and allows investigation of antigen-specific B cells, and GC B and T cell response for the first time. Mechanistic studies of regulatory and effector responses to influence antibody development are ongoing. Together, data makes fundamental insights into germinal centre responses during human malaria infection and allow pathways to improve vaccine immunogenicity in target populations.  

All welcome!