Causes of type 1 diabetes revealed?

Sometimes known as "early onset diabetes" or "juvenile diabetes", Type 1 diabetes is an autoimmune disease where the body attacks and destroys its own insulin-producing cells. It obliges patients to maintain blood glucose monitoring and an insulin-injecting regimen for the rest of their lives.

There are said to be two immune cells that are critically involved in most autoimmune disease: B cells, which make antibodies, and T cells, which kill cells infected with microbes or other invaders. In Type 1 diabetes, B cells start to see insulin-producing beta cells in the pancreas as "the enemy", and recruit T cells to kill these cells.

Now, an international team, led by Lewis Cox and Pablo Silveira of Sydney’s Garvan Institute of Medical Research, has identified two chromosomal regions that control the ability of beta cell reactive B cells to interact with T cells, and determine whether or not Type 1 diabetes develops.

The study on mice has been published in 'The European Journal of Immunology'.
"In any disease process, our T cells and B cells communicate with each other by sending signals. 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.

"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'," Silveira said.

He added: "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."