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Garvan Institute

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Mucosal Autoimmunity

 

Cecile King's lab is interested mucosal autoimmunity. In type 1 diabetes (T1D), the insulin-producing beta cells of the pancreas are destroyed by selftissue- destructive T cells. These cells express markers that help us to determine, for example, their dependence upon growth factors and where they have been in the body. We are particularly interested in the relationship between the cells that cause T1D and other autoimmune diseases that develop at the mucosal interface between our bodies and the environment. Broad-based suppression is commonly used to treat autoimmune diseases and transplant recipients but it has an obvious drawback since we need a functioning immune system in order to thrive. The aim of our research is to identify target molecules for selective suppression of these self-tissue-destructive cells. 

 

 

Staff

 

Helen McguireResearch Officer
Helen McGuire
Joanna WarrenResearch Assistant
Joanna Warren
Claudia LoetschPhD Student
Claudia Loetsch
Visiting Student
Sylvie Denoyelle

 

 

 

News

 

Breakthrough study links Type 1 diabetes and Sjogren’s syndrome

MEDIA RELEASE: 22 Apr 2011
Garvan scientists have identified a new group of immune cells that for the first time directly link two autoimmune diseases, Type 1 diabetes and Sjogren’s syndrome. Autoimmune diseases arise when the body’s defences become overactive, and instead of attacking invading microbes, it starts to attack itself. In the case of Type 1 diabetes, the body attacks insulin-producing cells in the pancreas. In the case of Sjogren’s syndrome, it attacks its own salivary glands.
 
 

Potential anti-rejection drug for insulin cell transplantation

MEDIA RELEASE: 01 Mar 2011
Garvan scientists have developed a reagent with the potential to prevent rejection of transplanted insulin-producing cells into people with Type 1 diabetes – one of the most promising immunology developments in recent years.
 
 

The genetic fuse that may ignite Type 1 diabetes

MEDIA RELEASE: 20 Oct 2009
Garvan scientists have discovered that a tiny genetic irregularity, which boosts the expression of a key gene, may lead to the development of Type 1 diabetes. While there is no cure yet, prevention therapies are on the horizon, making the development of reliable screening tools critical. And that's where the current finding has promise.
 
 

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