Professor Emma Hamilton-Williams
Professor

Emma Hamilton-Williams

Email: 
Phone: 
+61 7 344 36989

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

Fields of research

Autoimmunity Biochemistry and cell biology Bioinformatics and computational biology Biological Sciences Biomedical and Clinical Sciences Cellular immunology Genetic immunology Genetics Immunology Medical microbiology Medical microbiology not elsewhere classified Proteomics and metabolomics Systems biology

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.

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

71 works between 2001 and 2025
All (71) Journal Article (57) Book Chapter (2) Conference Publication (12)

41 - 60 of 71 works

2016

Journal Article

Reduced interleukin-2 responsiveness impairs the ability of Treg cells to compete for IL-2 in nonobese diabetic mice

James, Cini R., Buckle, Irina, Muscate, Franziska, Otsuka, Masayuki, Nakao, Mari, Oon, Jack S. H., Steptoe, Raymond J., Thomas, Ranjeny and Hamilton-Williams, Emma E. (2016). Reduced interleukin-2 responsiveness impairs the ability of Treg cells to compete for IL-2 in nonobese diabetic mice. Immunology and Cell Biology, 94 (5), 509-519. doi: 10.1038/icb.2016.7

Reduced interleukin-2 responsiveness impairs the ability of Treg cells to compete for IL-2 in nonobese diabetic mice

2016

Conference Publication

Type 1 diabetes susceptibility genes impair gut physiology and lead to perturbations in the microbiota

Mullaney, J., Stephens, J. and Hamilton-Williams, E. (2016). Type 1 diabetes susceptibility genes impair gut physiology and lead to perturbations in the microbiota. International Congress of Immunology (ICI), Melbourne, Australia, Aug 21-26, 2016. Weinheim, Germany: Wiley - V C H Verlag GmbH & Co. KGaA. doi: 10.1002/eji.201670200

Type 1 diabetes susceptibility genes impair gut physiology and lead to perturbations in the microbiota

2016

Conference Publication

Development of a model for antigen-specific tolerising immunotherapy and response in NOD mice

Buckle, I, Steptoe, R. J., Thomas, R. and Hamilton-Williams, E. E. (2016). Development of a model for antigen-specific tolerising immunotherapy and response in NOD mice. International Congress of Immunology (ICI 2016), Melbourne, Australia, 21-26 August 2016. Weinheim, Germany: Wiley.

Development of a model for antigen-specific tolerising immunotherapy and response in NOD mice

2015

Journal Article

Expression profiling pre-diabetic mice to uncover drugs with clinical application to type 1 diabetes

Pang, Dimeng, Irvine, Katharine M., Mehdi, Ahmed M., Thomas, Helen E., Harris, Mark, Hamilton-Williams, Emma E. and Thomas, Ranjeny (2015). Expression profiling pre-diabetic mice to uncover drugs with clinical application to type 1 diabetes. Clinical and Translational Immunology, 4 (8) e41, e41.1-e41.9. doi: 10.1038/cti.2015.17

Expression profiling pre-diabetic mice to uncover drugs with clinical application to type 1 diabetes

2013

Journal Article

Fine mapping of type 1 diabetes regions Idd9.1 and Idd9.2 reveals genetic complexity

Hamilton-Williams, Emma E., Rainbow, Daniel B., Cheung, Jocelyn, Christensen, Mikkel, Lyons, Paul A., Peterson, Laurence B., Steward, Charles A., Sherman, Linda A. and Wicker, Linda S. (2013). Fine mapping of type 1 diabetes regions Idd9.1 and Idd9.2 reveals genetic complexity. Mammalian Genome, 24 (9-10), 358-375. doi: 10.1007/s00335-013-9466-y

Fine mapping of type 1 diabetes regions Idd9.1 and Idd9.2 reveals genetic complexity

2013

Journal Article

Genetic interactions among Idd3, Idd5.1, Idd5.2, and Idd5.3 protective loci in the nonobese diabetic mouse model of type 1 diabetes

Lin, Xiaotian, Hamilton-Williams, Emma E., Rainbow, Daniel B., Hunter, Kara M., Dai, Yang D., Cheung, Jocelyn, Peterson, Laurence B., Wicker, Linda S. and Sherman, Linda A. (2013). Genetic interactions among Idd3, Idd5.1, Idd5.2, and Idd5.3 protective loci in the nonobese diabetic mouse model of type 1 diabetes. Journal of Immunology, 190 (7), 3109-3120. doi: 10.4049/jimmunol.1203422

Genetic interactions among Idd3, Idd5.1, Idd5.2, and Idd5.3 protective loci in the nonobese diabetic mouse model of type 1 diabetes

2012

Journal Article

PTPN22 alters the development of regulatory T cells in the thymus

Maine, Christian J., Hamilton-Williams, Emma E., Cheung, Jocelyn, Stanford, Stephanie M., Bottini, Nunzio, Wicker, Linda S. and Sherman, Linda A. (2012). PTPN22 alters the development of regulatory T cells in the thymus. Journal of Immunology, 188 (11), 5267-5275. doi: 10.4049/jimmunol.1200150

PTPN22 alters the development of regulatory T cells in the thymus

2012

Journal Article

Cellular mechanisms of restored β-cell tolerance mediated by protective alleles of Idd3 and Idd5

Hamilton-Williams, Emma E., Cheung, Jocelyn, Rainbow, Daniel B., Hunter, Kara M., Wicker, Linda S. and Sherman, Linda A. (2012). Cellular mechanisms of restored β-cell tolerance mediated by protective alleles of Idd3 and Idd5. Diabetes, 61 (1), 166-174. doi: 10.2337/db11-0790

Cellular mechanisms of restored β-cell tolerance mediated by protective alleles of Idd3 and Idd5

2011

Journal Article

Insulinoma-released exosomes or microparticles are immunostimulatory and can activate autoreactive T cells spontaneously developed in nonobese diabetic mice

Sheng, Huiming, Hassanali, Saleena, Nugent, Courtney, Wen, Li, Hamilton-Williams, Emma, Dias, Peter and Dai, Yang D. (2011). Insulinoma-released exosomes or microparticles are immunostimulatory and can activate autoreactive T cells spontaneously developed in nonobese diabetic mice. Journal of Immunology, 187 (4), 1591-1600. doi: 10.4049/jimmunol.1100231

Insulinoma-released exosomes or microparticles are immunostimulatory and can activate autoreactive T cells spontaneously developed in nonobese diabetic mice

2011

Conference Publication

Exosome-like microparticles can stimulate both innate and adaptive autoimmunity in non-obese diabetes mice

Dai, Yang, Sheng, Huiming, Hassanali, Saleema, Nugent, Courtney, Wen, Li, Hamilton-Williams, Emma and Dias, Peter (2011). Exosome-like microparticles can stimulate both innate and adaptive autoimmunity in non-obese diabetes mice. AMER ASSOC IMMUNOLOGISTS.

Exosome-like microparticles can stimulate both innate and adaptive autoimmunity in non-obese diabetes mice

2010

Journal Article

Idd9.2 and Idd9.3 Protective Alleles Function in CD4(+) T-Cells and Nonlymphoid Cells to Prevent Expansion of Pathogenic Islet-Specific CD8(+) T-Cells

Hamilton-Williams, Emma E., Wong, S.B. Justin, Martinez, Xavier, Rainbow, Daniel B., Hunter, Kara M., Wicker, Linda S. and Sherman, Linda A. (2010). Idd9.2 and Idd9.3 Protective Alleles Function in CD4(+) T-Cells and Nonlymphoid Cells to Prevent Expansion of Pathogenic Islet-Specific CD8(+) T-Cells. Diabetes, 59 (6), 1478-1486. doi: 10.2337/db09-1801

Idd9.2 and Idd9.3 Protective Alleles Function in CD4(+) T-Cells and Nonlymphoid Cells to Prevent Expansion of Pathogenic Islet-Specific CD8(+) T-Cells

2009

Journal Article

Expression of diabetes-associated genes by dendritic cells and CD4 T cells drives the loss of tolerance in nonobese diabetic mice

Hamilton-Williams, Emma E., Martinez, Xavier, Clark, Jan, Howlett, Sarah, Hunter, Kara M., Rainbow, Daniel B., Wen, Li, Shlomchik, Mark J., Katz, Jonathan D., Beilhack, Georg F., Wicker, Linda S. and Sherman, Linda A. (2009). Expression of diabetes-associated genes by dendritic cells and CD4 T cells drives the loss of tolerance in nonobese diabetic mice. Journal of Immunology, 183 (3), 1533-1541. doi: 10.4049/jimmunol.0900428

Expression of diabetes-associated genes by dendritic cells and CD4 T cells drives the loss of tolerance in nonobese diabetic mice

2009

Journal Article

Correction to: Kidney dendritic cell activation is required for progression of renal disease in a mouse model of glomerular injury

Heymann, Felix, Meyer-Schwesinger, Catherine, Hamilton-Williams, Emma E., Hammerich, Linda, Panzer, Ulf, Kaden, Sylvia, Quaggin, Susan E., Floege, Jurgen, Grone, Hermann-Josef and Kurts, Christian (2009). Correction to: Kidney dendritic cell activation is required for progression of renal disease in a mouse model of glomerular injury. Journal of Clinical Investigation, 119 (7), 2114-2114. doi: 10.1172/JCI38399C1

Correction to: Kidney dendritic cell activation is required for progression of renal disease in a mouse model of glomerular injury

2009

Journal Article

Kidney dendritic cell activation is required for progression of renal disease in a mouse model of glomerular injury

Heymann, Felix, Meyer-Schwesinger, Catherine, Hamilton-Williams, Emma E., Hammerich, Linda, Panzer, Ulf, Kaden, Sylvia, Quaggin, Susan E., Floege, Jurgen, Grone, Hermann-Josef and Kurts, Christian (2009). Kidney dendritic cell activation is required for progression of renal disease in a mouse model of glomerular injury. Journal of Clinical Investigation, 119 (5), 1286-1297. doi: 10.1172/JCI38399

Kidney dendritic cell activation is required for progression of renal disease in a mouse model of glomerular injury

2009

Conference Publication

Antigen-specific suppression of non-lymphoid tissue auto-antibody production by CD25(+) FoxP3(+) regulatory T cells

Kurts, Christian, Ludwig-Portugall, Isis, Hamilton-Williams, Emma E., Gottschalk, Catherine and Gotot, Janine (2009). Antigen-specific suppression of non-lymphoid tissue auto-antibody production by CD25(+) FoxP3(+) regulatory T cells. BETHESDA: AMER ASSOC IMMUNOLOGISTS.

Antigen-specific suppression of non-lymphoid tissue auto-antibody production by CD25(+) FoxP3(+) regulatory T cells

2009

Journal Article

CD25(+) T-reg specifically suppress auto-Ab generation against pancreatic tissue autoantigens

Ludwig-Portugall, Isis, Hamilton-Williams, Emma E., Gotot, Janine and Kurts, Christian (2009). CD25(+) T-reg specifically suppress auto-Ab generation against pancreatic tissue autoantigens. European Journal of Immunology, 39 (1), 225-233. doi: 10.1002/eji.200838699

CD25(+) T-reg specifically suppress auto-Ab generation against pancreatic tissue autoantigens

2009

Conference Publication

Expression of the Diabetes Associated Alleles of ldd3 and ldd5 in DCs Drives Loss of Tolerance in NOD Mice

Hamilton-Williams, Emma E., Martinez, Xavier, Hunter, Kara M., Rainbow, Dan, Wicker, Linda S. and Sherman, Linda A. (2009). Expression of the Diabetes Associated Alleles of ldd3 and ldd5 in DCs Drives Loss of Tolerance in NOD Mice. 9th Annual Meeting of the Federation-of-Clinical-Immunology-Societies, San Francisco Ca, Jun 11-14, 2009. SAN DIEGO: ACADEMIC PRESS INC ELSEVIER SCIENCE. doi: 10.1016/j.clim.2009.03.270

Expression of the Diabetes Associated Alleles of ldd3 and ldd5 in DCs Drives Loss of Tolerance in NOD Mice

2008

Journal Article

Cutting edge: CD25(+) regulatory T cells prevent expansion and induce apoptosis of B cells specific for tissue autoantigens

Ludwig-Portugall, Isis, Hamilton-Williams, Emma E., Gottschalk, Catherine and Kurts, Christian (2008). Cutting edge: CD25(+) regulatory T cells prevent expansion and induce apoptosis of B cells specific for tissue autoantigens. Journal of Immunology, 181 (7), 4447-4451. doi: 10.4049/jimmunol.181.7.4447

Cutting edge: CD25(+) regulatory T cells prevent expansion and induce apoptosis of B cells specific for tissue autoantigens

2008

Conference Publication

CD8 T cells specific for a glomerular antigen induce renal inflammation in a CD4 help dependent fashion and may cause progressing Glomerulonephritis

Heymann, F., Hamilton-Williams, E. E., Ludwig-Portugall, I., Quaggin, S., Floege, J., Groene, H. and Kurts, C. (2008). CD8 T cells specific for a glomerular antigen induce renal inflammation in a CD4 help dependent fashion and may cause progressing Glomerulonephritis. SPRINGER WIEN.

CD8 T cells specific for a glomerular antigen induce renal inflammation in a CD4 help dependent fashion and may cause progressing Glomerulonephritis

2008

Conference Publication

Restoration of CD8 self-tolerance in NOD mice by protective Idd9 genes

Hamilton-Williams, Emma, Martinez, Javier, Wong, Justin, Wicker, Linda and Sherman, Linda (2008). Restoration of CD8 self-tolerance in NOD mice by protective Idd9 genes. FEDERATION AMER SOC EXP BIOL.

Restoration of CD8 self-tolerance in NOD mice by protective Idd9 genes

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

Availability

Professor Emma Hamilton-Williams is:
Available for supervision

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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

Enquiries

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

  • autoimmunity
  • immunotherapy
  • microbiome
  • type 1 diabetes

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