Insight into how immune cells cause diabetes
Wednesday, 27 October, 2010
Researchers from Sydney's Garvan Institute of Medical Research have uncovered a mechanism by which immune cells interact, giving insight into the causes of Type 1 diabetes, where the body's own immune cells target the insulin-producing beta cells in the pancreas.
According to Garvan researcher, Dr Pablo Silveira, B cells and T cells - both fundamental to our adaptive immune system - communicate with each other in order to coordinate their response.
“In any disease process, our T cells and B cells communicate with each other by sending signals,” said Silveira.
“Sometimes those signals say ‘I’m going to co-operate with you’, and sometimes they don’t. You can think of it as one type of cell saying to the other ‘let’s dance!’ with the potential partner either accepting or declining.”
Silveria and Dr Lewis Cox identified two regions on the chromosomes of mice that influence this process.
They found that these regions influence certain B cells that naturally target the body's insulin-producing beta cells to become more receptive to T cells, resulting in them attacking beta cells, causing Type 1 diabetes.
“In people or animals with Type 1 diabetes susceptibility genes, B cells targeting beta cells become more promiscuous or receptive, and accept the T cell invitation to dance. In healthy people or animals, these B cells say ‘no thanks’," said Silveria.
“If the pair dance together, they proliferate and become lethal, resulting in a concerted attack against the beta cells. Without that dance, and in this case it’s the co-operation of B cells that matters, the disease cannot progress.
“We looked at B cells recognising beta cells from healthy mice and from mice with a genetic predisposition to developing diabetes. Each received the same type of T cell help, but the B cells responded very differently, showing us that the genes involved are B cell intrinsic.”
The discovery, published in The European Journal of Immunology, will hopefully provide clues as to targets for therapeutics that can manipulate the communication between B cells and T cells, thus preventing Type 1 diabetes.
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