Dr Emma Hamilton-Williams
Dr Emma Hamilton-Williams

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The research passion of Dr Emma Hamilton-Williams, Research Fellow at The University of Queensland Diamantina Institute (UQDI), is type 1 diabetes (T1D), an autoimmune disease that ultimately leads to the destruction of the insulin producing β-cells.

T1D was once called ‘juvenile onset diabetes’, since most patients are diagnosed in early childhood and will depend on insulin injections for the rest of their lives. In Australia, more than two people are newly diagnosed with this disease every day, and the rate is increasing by almost 3% each year. Despite worldwide research efforts, the cause of T1D is still unknown. Researchers have identified several genetic factors that predispose for T1D, but a trigger that sets off the autoimmune events has not unequivocally been found.

Drawn to biological sciences at an early age through the influence of her mother, a botanist and electron microscopist, Hamilton-Williams completed her undergraduate education at the Victoria University of Wellington, New Zealand. Her interest in genetics and human disease was sparked during her honours year researching a congenital disease that affects the adrenal gland. Hamilton-Williams then went on to do a PhD at the John Curtin School of Medical Research (Australian National University, Canberra), where she used cutting edge gene technology to create new research models for T1D.

Her first postdoctoral position took Hamilton-Williams to the laboratory of Professor Christian Kurts in Germany. Her studies there focussed on how particular immune cells (called T-cells) maintain their tolerance towards the body’s own tissue, which provided new insights into the triggers for autoimmunity disorders, including T1D.

Hamilton-Williams then moved to The Scripps Research Institute in California for further postdoctoral research into diabetes, this time looking at T1D susceptibility genes and how they modulate the immune response on a cellular level. She found that mutations in a certain T1D susceptibility gene not only affected T-cells, as believed at that time, but also another type of immune cells called dendritic cells – a discovery that has direct impact on current T1D therapies.

The wish to be closer to her family and provide her children with an Australian lifestyle and education prompted Hamilton-Williams to move back to Australia in 2011. Eager to continue her research into the detailed effects of T1D promoting genes on the body’s immune system, she joined UQDI for the Institute’s close fit with her research goals and the opportunity to collaborate with world leaders in autoimmunity, genetics and dendritic cell biology.

Hamilton-Williams’ current research aims are two-fold: on one hand she strives to understand the potential protective effects that dendritic cells can provide at certain stages of T1D progression. On the other hand, she aims to unravel the links between T1D susceptibility genes and environmental factors like the gut flora.

Hamilton-Williams is driven by a passion to understand complex diseases like T1D and to find ways to improve the lives of people who suffer from these diseases. The answers to her research questions certainly have the potential to make the prediction and prevention of T1D a reality, as well as change the way we treat the disease.

 

 

Email: e.hamiltonwilliams@uq.edu.au
Phone: +61 7 3443 6989

 

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Recent publiations

Pang D, Irvine KM, Mehdi AM, Thomas HE, Harris M, Hamilton-Williams EE* and Thomas R*. Expression profiling pre-diabetic mice to uncover drugs with clinical application to type 1 diabetes. Clinical & Translational Immunology. In Press.

Lin X, Hamilton-Williams EE*, Rainbow DB, Hunter KM, Dai YD, Cheung J, Peterson LB, Wicker LS and Sherman LA. Genetic interactions among Idd3, Idd5.1, Idd5.2 and Idd5.3 protective loci in the NOD mouse model of type 1 diabetes. J. Immunol. 2013 Accepted for publication

Maine C, Hamilton-Williams EE, Cheung J, Bottini N, Wicker LS and Sherman LA. PTPN22 alters the development and homeostasis of T regulatory cells in the thymus and periphery. J. Immunol. 2012, epub 25 April doi: 10.4049/jimmunol.1200150

Hamilton-Williams EE, Cheung J, Rainbow DB, Hunter KM, Wicker LS, and Sherman LA. Cellular mechanisms of restored β cell tolerance mediated by protective alleles of Idd3 and Idd5. Diabetes. 2012, 61(1):166-74.

Sheng H, Hassanali S, Nugent C, Wen L, Hamilton-Williams E, Dias P and Dai YD. Insulinoma-released exosomes or microparticles are immunostimulatory and can activate autoreactive T cells spontaneously developed in nonobese diabetic mice. J Immunol. 2011 Aug 15;187(4):1591-600.

Hamilton-Williams EE, Wong JSB, Martinez X, Rainbow DB, Hunter KM, Wicker LS, and Sherman LA. Idd9.2 and Idd9.3 protective alleles function in CD4+ T-cells and a non-lymphoid cell to prevent expansion of pathogenic islet specific CD8+ T-cells. Diabetes. 2010, 59(6): 1478-86.

Hamilton-Williams EE, Martinez X, Clark J, Howlett S, Hunter KM, Rainbow DB, Wen L, Shlomchik MJ, Katz JD, Beilhack GF, Wicker LS and Sherman LA. Expression of diabetes-associated genes by dendritic cells and CD4 T-cells drives the loss of tolerance in nonobese diabetic mice. J. Immunol 2009, 183:1533-41.

Heymann F, Meyer-Schwesinger C, Hamilton-Williams EE, Hammerich L, Panzer U, Kaden S, Quaggin SE, Floege J, Gröne HJ and Kurts C. Kidney dendritic cell activation is required for progression of renal disease in a mouse model of glomerular injury. J Clin Invest. 2009, 119:1286-97.

Ludwig-Portugall I, Hamilton-Williams EE, Gotot J and Kurts C. CD25+ regulatory T cells specifically suppress auto-antibody generation against pancreatic tissue autoantigens. Eur. J. Immunol, 2009, 39:225-33

Ludwig-Portugall I, Hamilton-Williams EE, Gottschalk C, and Kurts C. CD25+ Regulatory T Cells Prevent Expansion and Induce Apoptosis of B Cells Specific for Tissue Autoantigens. J Immunol, 2008, 181:4447-51.

Hamilton-Williams EE, Martinez X, Lyman MA, Hunter K, Wicker LS and Sherman LA. The Use Of Idd Congenic Mice to Identify Checkpoints of Peripheral Tolerance to Islet Antigen. Ann N Y Acad Sci. 2007, 1103: 118-27.


 

 

 

  • A novel role for the interleukin-2 pathway in humans and mouse models of type 1 diabetes
  • Genetic control of intestinal microflora in type 1 diabetes susceptibility
  • Impaired Regulatory T cell function in type 1 diabetes