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Walter & Eliza Hall Institute
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Autoimmunity and Transplantation

2004-2005


Research Overview | Research Divisions | Online Resources | Collaborative Research

Cancer & Haematology | Molecular Genetics of Cancer | Immunology | Infection & Immunity
Autoimmunity & Transplantion
| Genetics & Bioinformatics | Structural Biology
From left: Len Harrison (Head), Bob Anderson, Margo Honeyman, Andrew Lew & Ian Wicks.


Clinical Links

The Autoimmunity and Transplantation Division has strong clinical and translational research links with the Royal Melbourne Hospital and elsewhere. Click on one of the links below to find out more about clinical research into type 1 diabetes and LADA, coeliac disease, and rheumatoid arthritis

Research Focus

  • Type 1 diabetes – clinical research
  • Type 1 diabetes – T cells
  • Pancreas development
  • Immune mechanisms
  • Rheumatoid arthritis
  • Coeliac disease

Overview

The central question in immunology is how the immune system maintains tolerance to ‘self’ while reacting to ‘non-self’ (eg microbial pathogens) or ‘altered self’ (eg tumours). When there is a breakdown in tolerance to ‘self’ the immune system may attack the body’s own tissues causing autoimmune disease. If the insulin-producing β cells in the pancreas are attacked the result is type 1 diabetes; if the joints are attacked the result is rheumatoid arthritis. In addition to these two common autoimmune diseases, we study a chronic inflammatory disease of the small bowel, coeliac disease, that occurs when the immune system reacts against the gluten protein in wheat. We aim to identify the genetic and environmental factors that lead to these diseases and, with the help of mouse models, understand the immune processes involved in order to prevent or ameliorate disease in humans. In addition, we are investigating ways to improve transplantation to replace damaged cells or tissues. Basic and clinical science interweave to provide new insights, with an emphasis on translation into clinical practice.

In a recent trial in children at high risk of type 1 diabetes, we found that an intranasal insulin vaccine resulted in immune and metabolic changes suggesting protection against diabetes development. A large, multicentre follow-up trial to determine if the vaccine prevents diabetes is about to commence. We have discovered that a modification in the structure of insulin activates aggressive immune T cells involved in type 1 diabetes. By examining gene expression, we discovered a novel receptor on β cells which could be involved in protecting the cells from immune attack. In rheumatoid arthritis, the suppressor of cytokine synthesis 3 protein (SOCS) was found to be vital in reducing inflammatory arthritis. In coeliac disease, parts of the gluten protein have been identified that activate T cells in disease, the first step towards a vaccine for disease prevention.


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Updated 02:50 PM (EST) on Friday, January 6, 2006.