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Professor Emma Hamilton-Williams
Professor

Emma Hamilton-Williams

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+61 7 344 36989

Overview

Background

Associate Professor Emma Hamilton-Williams’ career focuses on understanding how immune tolerance is disrupted leading to the development of the autoimmune disease type 1 diabetes. She received her PhD from the Australian National University in 2001, followed by postdoctoral training in Germany and the Scripps Research Institute in the USA.

In 2012, she started a laboratory at the Frazer Institute, University of Queensland where she investigates the gut microbiota as a potential trigger or therapy target for type 1 diabetes, as well as developing an immunotherapy for type 1 diabetes. The overall aim of her research is to find new ways to prevent or treat the underlying immune dysfunction causing autoimmunity.

She is Chief Scientific Officer for an Australia-wide pregnancy-birth cohort study of children at increased risk of type 1 diabetes, which aims to uncover the environmental drivers of this disease. Her laboratory uses big-data approaches including proteomics, metabolomics and metagenomics to understand the function of the gut microbiota linked to disease.

She recently conducted a clinical trial of a microbiome-targeting biotherapy aimed at restoring a healthy microbiome and immune tolerance, with an ultimate aim of preventing type 1 diabetes.

Availability

Professor Emma Hamilton-Williams is:
Available for supervision
Media expert

Qualifications

  • Bachelor (Honours) of Science (Advanced), Victoria University of Wellington
  • Doctor of Philosophy, Australian National University

Research interests

  • The gut microbiome as a trigger for type 1 diabetes

    This theme focuses on understanding disease pathogenesis in type 1 diabetes with a focus on the gut microbiota. We have pioneered the use of metaproteomics to understand host-microbiota interactions in type 1 diabetes. We are using this approach to uncover novel biomarkers associated with intestinal inflammation in type 1 diabetes and to monitor therapeutic response in gut microbiota targeted clinical trials. We are using several approaches such as metagenomics, metabolomics, in vitro assays and fecal microbiome transplant studies to understand the function of the gut microbiota linked to disease.

  • Gut-microbiota directed interventions for prevention of type 1 diabetes

    Type 1 diabetes incidence is rising due to changing environmental drivers such as the gut microbiota. We are investigating whether restoration of beneficial microbes is a potential preventative therapy for type 1 diabetes. We are investigating prebiotic diet based therapies and probiotic approaches as well as metabolite delivery to remodel the gut microbiota and restore immune tolerance to ultimately prevent type 1 diabetes.

  • Immunotherapy for type 1 diabetes

    The Hamilton-Williams lab is currently using liposomal nanoparticles to develop a vaccine to specifically prevent or treat type 1 diabetes. Liposomes are a safe and tailorable vehicle to deliver immune-modulating drugs and antigen in order to induce tolerance in islet-specific T cells. Our current work is optimising the delivery route, frequency, antigen and adjunct therapies in order to maximise disease protection from our immunotherapy. We are using humanised models to test our approach. This immunotherapy is being translated for human use with the first clinical trial starting in 2024

Research impacts

A/Prof Hamilton-Williams early work demonstrated how cytotoxic T cells initiate the attack on the insulin-producing cells in the pancreas, leading to type 1 diabetes. She showed how a number of genes linked to genetic risk for type 1 diabetes changed immune cell function causing loss of self-tolerance.

More recently, she has co-led a clinical trial of a microbiome-targeted biotherapy in adults with type 1 diabetes. This pilot study demonstrated the safety and feasibility of this approach, as well as providing preliminary evidence that the therapy was associated with positive changes in the gut microbiome, immune response and glucose control.

She is the Chief Scientific Officer of a study following ~1500 children who have a close family member with type 1 diabetes from pregnancy and through childhood. This study is unravelling the underlying drivers of type 1 diabetes including the relationship between autoimmunity and the gut microbiome, viral infections, diet and many other lifestyle factors.

A/Prof Hamilton-Williams is collaborating with other UQ researchers to develop an new immunotherapy for type 1 diabetes. She has led studies demonstrating the efficacy of the approach and unravelling the underlying mechanisms in preclinical models. This therapy is now being tested in a first-in-human clinical trial in adults with type 1 diabetes.

Works

Search Professor Emma Hamilton-Williams’s works on UQ eSpace

70 works between 2001 and 2024

61 - 70 of 70 works

2006

Journal Article

Inclusion of Brefeldin A during dendritic cell isolation allows in vitro detection of cross-presented self-antigens

Benke, Dirk, Kruger, Thilo, Lang, Andreas, Hamilton-Williams, Emma E. and Kurts, Christian (2006). Inclusion of Brefeldin A during dendritic cell isolation allows in vitro detection of cross-presented self-antigens. Journal of Immunological Methods, 310 (1-2), 12-19. doi: 10.1016/j.jim.2005.10.019

Inclusion of Brefeldin A during dendritic cell isolation allows in vitro detection of cross-presented self-antigens

2006

Book Chapter

Influence of toll-like receptor ligands and danger signals on T cell cross-tolerance

Hamilton-Williams, E. E. and Kurts, C. (2006). Influence of toll-like receptor ligands and danger signals on T cell cross-tolerance. Towards an understanding of initiating T cell immunity. (pp. 147-168) edited by Anthony T. Vella. Kerala, India: Research Signpost.

Influence of toll-like receptor ligands and danger signals on T cell cross-tolerance

2005

Journal Article

Cutting edge: TLR ligands are not sufficient to break cross-tolerance to self-antigens

Hamilton-Williams, Emma E., Lang, Andreas, Benke, Dirk, Davey, Gayle M., Wiesmuller, Karl-Heinz and Kurts, Christian (2005). Cutting edge: TLR ligands are not sufficient to break cross-tolerance to self-antigens. Journal of Immunology, 174 (3), 1159-1163. doi: 10.4049/jimmunol.174.3.1159

Cutting edge: TLR ligands are not sufficient to break cross-tolerance to self-antigens

2005

Journal Article

Heat shock protein 60 is released in immune-mediated glomerulonephritis and aggravates disease: In vivo evidence for an immunologic danger signal

Lang, Andreas, Benke, Dirk, Eitner, Frank, Engel, Daniel, Ehrlich, Svenja, Breloer, Minka, Hamilton-Williams, Emma, Specht, Sabine, Hoerauf, Achim, Floege, Jürgen, von Bonin, Arne and Kurts, Christian (2005). Heat shock protein 60 is released in immune-mediated glomerulonephritis and aggravates disease: In vivo evidence for an immunologic danger signal. Journal of the American Society of Nephrology, 16 (2), 383-391. doi: 10.1681/ASN.2004040276

Heat shock protein 60 is released in immune-mediated glomerulonephritis and aggravates disease: In vivo evidence for an immunologic danger signal

2004

Journal Article

Identification and functional characterization of dendritic cells in the healthy murine kidney and in experimental glomerulonephritis

Kruger, T, Benke, D, Eitner, F, Lang, A, Wirtz, M, Hamilton-Williams, EE, Engel, D, Giese, B, Muller-Newen, G, Floege, J and Kurts, C (2004). Identification and functional characterization of dendritic cells in the healthy murine kidney and in experimental glomerulonephritis. Journal of the American Society of Nephrology, 15 (3), 613-621. doi: 10.1097/01.ASN.0000114553.36258.91

Identification and functional characterization of dendritic cells in the healthy murine kidney and in experimental glomerulonephritis

2003

Conference Publication

Release of heat shock protein 60 is an endogenous enhancer of nephrotoxic nephritis

Kurts, C, Lang, A, Kruger, T, Benke, D, Hamilton-Williams, E, Wirtz, M, Ehrlich, S, von Bonin, A, Assmann, K, Eitner, F and Floege, J (2003). Release of heat shock protein 60 is an endogenous enhancer of nephrotoxic nephritis. 36th Annual Meeting of the American-Society-of-Nephrology, San Diego California, Nov 12-17, 2003. LIPPINCOTT WILLIAMS & WILKINS.

Release of heat shock protein 60 is an endogenous enhancer of nephrotoxic nephritis

2003

Journal Article

Beta cell MHC class I is a late requirement for diabetes

Hamilton-Williams, EE, Palmer, SE, Charlton, B and Slattery, RM (2003). Beta cell MHC class I is a late requirement for diabetes. Proceedings of the National Academy of Sciences of the United States of America, 100 (11), 6688-6693. doi: 10.1073/pnas.1131954100

Beta cell MHC class I is a late requirement for diabetes

2003

Journal Article

Development of new strategies to prevent type diabetes: the role of animal models

Hanninen, A, Hamilton-Williams, E and Kurts, C (2003). Development of new strategies to prevent type diabetes: the role of animal models. Annals of Medicine, 35 (8), 546-563. doi: 10.1080/07853890310014597

Development of new strategies to prevent type diabetes: the role of animal models

2002

Journal Article

Acute reversible renal failure in acute generalized exanthematous pustulosis

Brandenburg, VM, Kurts, C, Eitner, F, Hamilton-Williams, E and Heintz, B (2002). Acute reversible renal failure in acute generalized exanthematous pustulosis. Nephrology Dialysis Transplantation, 17 (10), 1857-1858. doi: 10.1093/ndt/17.10.1857

Acute reversible renal failure in acute generalized exanthematous pustulosis

2001

Journal Article

Transgenic rescue implicates beta(2)-microglobulin as a diabetes susceptibility gene in nonobese diabetic (NOD) mice

Hamilton-Williams, EE, Serreze, DV, Charlton, B, Johnson, EA, Marron, MP, Mullbacher, A and Slattery, RM (2001). Transgenic rescue implicates beta(2)-microglobulin as a diabetes susceptibility gene in nonobese diabetic (NOD) mice. Proceedings of the National Academy of Sciences of the United States of America, 98 (20), 11533-11538. doi: 10.1073/pnas.191383798

Transgenic rescue implicates beta(2)-microglobulin as a diabetes susceptibility gene in nonobese diabetic (NOD) mice

Funding

Current funding

  • 2024 - 2026
    When is the critical window to intervene in early life to reduce the impact of overweight on the risk of type 1 diabetes? (Diabetes SA Grant led by The University of Adelaide)
    University of Adelaide
    Open grant
  • 2024 - 2025
    Deep milk: comprehensive multi-omics to resolve the role of human breastmilk in type 1 diabetes risk (JDRF AU Accelerating Collab Research in T1D) administered by Baker Heart and Diabetes Institute
    Baker IDI Heart & Diabetes Institute
    Open grant
  • 2024 - 2027
    Targeting gut microbial metabolites to prevent type 1 diabetes
    NHMRC IDEAS Grants
    Open grant
  • 2023 - 2025
    Gut microbial metabolites during early-life development as predictors of islet autoimmunity
    The Leona M. and Harry B. Helmsley Charitable Trust
    Open grant
  • 2023 - 2025
    Early environmental determinants of pancreatic islet autoimmunity (ENDIA) Cohort Follow-up 2023-2025 (JDRF Australia grant led by University of Adelaide)
    University of Adelaide
    Open grant
  • 2021 - 2026
    Microbiota-targeted dietary intervention in children with type 1 diabetes
    Research Donation Generic
    Open grant

Past funding

  • 2023
    Gut microbial metabolites during early-life development as predicators of islet autoimmunity
    Diabetes Australia Research Program
    Open grant
  • 2021
    Specialized dietary intervention in children with type 1 diabetes (APEG Research Grant Administered by Queensland Children¿s Hospital)
    Children's Health Queensland Hospital and Health Service
    Open grant
  • 2021 - 2024
    Influence of early life and maternal host-microbiota interactions on type1 diabetes risk
    JDRF Australia and Helmsley Charitable Trust ENDIA Early-Mid Career Science Accelerator Awards
    Open grant
  • 2021 - 2024
    Tolerising antigen-specific immunotherapy for type 1 diabetes
    NHMRC IDEAS Grants
    Open grant
  • 2020 - 2022
    A specialised dietary supplement for manipulating the gut microbiota to treat type 1 diabetes
    The Children's Hospital Foundation
    Open grant
  • 2019 - 2023
    Crosstalk between host and intestinal microorganisms in progression to islet autoimmunity
    Juvenile Diabetes Research Foundation - International
    Open grant
  • 2018 - 2019
    Maintaining immune tolerance to prevent type 1 diabetes
    The Children's Hospital Foundation
    Open grant
  • 2018 - 2020
    Specialized dietary intervention in human type 1 diabetes (JDRF ELEVATE: Future Research Leaders Program 2018 Pilot Study led by Monash University)
    Monash University
    Open grant
  • 2018 - 2019
    Oral liposomes for antigen-specific immunotherapy of type 1 diabetes
    Diabetes Australia Research Trust
    Open grant
  • 2016
    The Australian human microbiota project-microbe isolation facility
    UQ Major Equipment and Infrastructure
    Open grant
  • 2015 - 2017
    Antigen-specific peptide immunotherapy targeting dendritic cells in type 1 diabetes
    Juvenile Diabetes Research Foundation - International
    Open grant
  • 2014 - 2016
    Host-Microbiota Interactions in Subjects at Risk for Type 1 Diabetes (JDRF Grant administered by University of Colorado)
    University of Colorado
    Open grant
  • 2013 - 2019
    A genetic link between gut microbial flora and T1D susceptibility
    Juvenile Diabetes Research Foundation
    Open grant
  • 2012 - 2016
    A novel role for the IL-2 pathway in type-1-diabetes.
    NHMRC Project Grant
    Open grant

Supervision

Availability

Professor Emma Hamilton-Williams is:
Available for supervision

Before you email them, read our advice on how to contact a supervisor.

Available projects

  • Gut microbiota-targeting to prevent type 1 diabetes

    We are using human cohort and intervention studies with a multi-omic analysis approach to understand how the host and microbiota interact in the lead-up to disease onset. We are using germ-free mice colonized with human derived microbiota or individual species to study how changes in the gut flora of patients may modify the immune response and lead to disease. Finally, we are investigating novel prebiotic diets for disease prevention.

  • Antigen-specific immunotherapy for type 1 diabetes

    We are investigating the use of a liposome system for antigen-specific immunotherapy in type 1 diabetes. Our goal is to restore tolerance in autoreactive islet-specific T cells. We are using multi-dimensional profiling of antigen-specific T cells to optimize our immunotherapy strategy. We also use CRSIPR/Cas9 systems to study the molecular mediators of regulation induced during immunotherapy.

  • Gut microbiota-targeting to prevent type 1 diabetes

    We are using human cohort and intervention studies with a multi-omic analysis approach to understand how the host and microbiota interact in the lead-up to disease onset. We are using germ-free mice colonized with human derived microbiota or individual species to study how changes in the gut flora of patients may modify the immune response and lead to disease. Finally, we are investigating novel prebiotic diets for disease prevention.

  • Antigen-specific immunotherapy for type 1 diabetes

    We are investigating the use of a liposome system for antigen-specific immunotherapy in type 1 diabetes. Our goal is to restore tolerance in autoreactive islet-specific T cells. We are using multi-dimensional profiling of antigen-specific T cells to optimize our immunotherapy strategy. We also use CRSIPR/Cas9 systems to study the molecular mediators of regulation induced during immunotherapy.

Supervision history

Current supervision

Completed supervision

Media

Enquiries

Contact Professor Emma Hamilton-Williams directly for media enquiries about:

  • autoimmunity
  • immunotherapy
  • microbiome
  • type 1 diabetes

Need help?

For help with finding experts, story ideas and media enquiries, contact our Media team:

communications@uq.edu.au