Dr Emma Hamilton-Williams

Senior Research Fellow

The University of Queensland Diamantina Institute
Faculty of Medicine

Overview

Dr Hamilton-Williams completed her PhD at the John Curtin School of Medical Research, Canberra in 2001 under the supervision of Dr Robyn Slattery. There she performed studies investigating the role of MHC class I expression and CD8+ T-cells in the pathogenesis of type 1 diabetes. These two studies both published in PNAS, identified beta-2-microglobulin as a type 1 diabetes susceptibility gene and demonstated that direct killing of islet beta cells by CD8+ was a requirement for diabetes development but not initiation of autoimmunity. She then undertook postdoctoral training in Germany to further study the mechanisms of tolerance induction in CD8+ T-cells. In 2005, she was awarded a Juvenile Diabetes Research Foundation (JDRF) postdoctoral fellowship and moved to the Scripps Research Institute in San Diego. There she continued to pursue her interest in the genetic control of CD8+ T-cell tolerance in type 1 diabetes. In 2012, she returned to Australia to set up her own laboratory at UQDI funded by the NHMRC and was recently awarded a Career Development Award from the JDRF.

Research Interests

  • Improving immunotherapy in type 1 diabetes
    Type 1 diabetes is caused by the immune mediated destruction of the insulin producing cells in the pancreas. Genes linked to susceptibility to disease are believed to alter the immune system, leading to a loss of tolerance to self-tissues such as the insulin producing cells in the pancreas. I am interested in restoring immune tolerance to the insulin producing cells by modulating the function of critical immune cells such as dendritic cells and regulatory T cells. We are investigating novel combination therapies aimed and improved deletion of auto reactive T cells and expansion of regulatory cell types.
  • The gut microbiome in type 1 diabetes
    Environmental factors play a large part in whether an individual develops type 1 diabetes, yet little is known about the precise nature of these factors. One possibility is that the bacteria resident in our gut influence the developing immune system and alter the likelihood of contracting type 1 diabetes. We are investigating whether gut bacteria differ between individuals with type 1 diabetes, their relatives and healthy people as well studying how the immune response to these bacteria may change.

Qualifications

  • Bachelor of Science with Honours, Victoria University of Wellington
  • Doctor of Philosophy, Australian National University

Publications

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Supervision

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Available Projects

  • Environmental factors such as diet and infections are thought to influence the development of type 1 diabetes. We are investigating the link between environment, the gut microbiota and predisposition to type 1 diabetes. This project will use a clinical cohort of stool samples to investigate changes in both human and microbiota derived factors that are associated with increasing risk of developing disease. Techniques to be used will include proteomics, bioinformatics and bacterial gene seqeuncing. The applicant should have some background in either protein chemistry, immunology or bioinformatics techniques.

  • Type 1 diabetes results from the loss of immune tolerance to the insulin producing cells in the pancreas. Development of immunotherapy stategies to either prevent or treat type 1 diabetes by deleting autoreactive T cells and improving long-lasting immune regulation are urgently needed for this disease. We am to trial novel combination therapies aimed at both inhibiting the activation of effector T cells and expanding regulatory T cells. In addition we are investigating antigen-sepcific approaches to specifically target the pathogenic T cells.

View all Available Projects

Publications

Book Chapter

Journal Article

Conference Publication

  • Hamilton-Williams, E.E., Martinez, X., Lyman, M., Hunter, K., Wicker, L.S. and Sherman, L.A. (2007). The use of Idd congenic mice to identify checkpoints of peripheral tolerance to islet antigen. In: Conference on How Do We Best Employ Animal Models for Type 1 Diabetes and Multiple Sclerosis, San Francisco, CA, United States, (118-127). 8-9 November 2006. doi:10.1196/annals.1394.003

Grants (Administered at UQ)

PhD and MPhil Supervision

Current Supervision

  • Doctor Philosophy — Principal Advisor

  • Doctor Philosophy — Principal Advisor

Possible Research Projects

Note for students: The possible research projects listed on this page may not be comprehensive or up to date. Always feel free to contact the staff for more information, and also with your own research ideas.

  • Environmental factors such as diet and infections are thought to influence the development of type 1 diabetes. We are investigating the link between environment, the gut microbiota and predisposition to type 1 diabetes. This project will use a clinical cohort of stool samples to investigate changes in both human and microbiota derived factors that are associated with increasing risk of developing disease. Techniques to be used will include proteomics, bioinformatics and bacterial gene seqeuncing. The applicant should have some background in either protein chemistry, immunology or bioinformatics techniques.

  • Type 1 diabetes results from the loss of immune tolerance to the insulin producing cells in the pancreas. Development of immunotherapy stategies to either prevent or treat type 1 diabetes by deleting autoreactive T cells and improving long-lasting immune regulation are urgently needed for this disease. We am to trial novel combination therapies aimed at both inhibiting the activation of effector T cells and expanding regulatory T cells. In addition we are investigating antigen-sepcific approaches to specifically target the pathogenic T cells.