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The Times has today (9 August 2012) covered a story about a potential role for the BCG vaccine in helping people with type 1. The story follows publication of an article in the journal PLoS One which claims to have shown benefit for a small number of people with long established type 1.

The study was led by Dr Denise Faustman of Massachusetts General Hospital, USA. Dr Faustman’s previous research in mice has shown that a molecule called TNF may help to turn off the immune response that leads to type 1 diabetes. As TNF cannot be safely administered to humans as a drug, the team have looked for other medications that can boost the body’s own levels of TNF. The BCG vaccine is known to increase levels of TNF in the body for a short time, so the team have conducted a small trial to see if this increase in TNF levels has an impact in people with type 1.

The study reported in the Times was published in the online journal PLoS One, and involved six patients. Three were given a placebo and three were given the BCG jab. Blood samples from two of the BCG patients showed that there was a small change in the balance between the ‘bad’ immune cells that target the insulin producing cells and the ‘good’ immune cells that work to supress autoimmune reactions in our bodies, for a short time after the trial. There was also evidence that the patients produced slightly more of their own insulin during this time. Unfortunately it was not enough to alter the way they managed their type 1. The same results were also seen in one of the patients who received the placebo, who had contracted a virus during the course of the study.

JDRF-funded researchers at the Karolinska Institute in Sweden have managed to stop the immune system attack on beta cells that causes type 1 in mice.

In the study which was published in the journal Diabetes this week, researchers found that injecting mice with immune cells called macrophages stopped the attack on beta cells.

Macrophages are a type of immune cell that can either protect cells from an immune attack or be the attacker, depending on which signals they receive from other cells around them.  The first part of this study, which was led by Dr Robert Harris, identified the signals that macrophages need to become protective.

The team were then able to use these signals to coax macrophages into the protective mode. The protective macrophages were then injected into mice whose immune system had begun to attack beta cells but were not yet insulin dependent.  Following the injection of macrophages, mice were less likely to develop type 1 and most could maintain their own insulin production.

 In type 1 diabetes, the immune system attacks the insulin producing cells in the pancreas. Finding a way to stop this attack early on may help to protect the remaining beta cells and allow people with the condition to continue producing at least some of their own insulin.

Maebh Kelly, Research Communication Officer at JDRF said ‘Understanding how cells in the immune system are directed to attack or defend other cells is an important step towards the development of immune therapies that can halt the development of type 1. Dr Harris’ research has provided us with new insight into the signals that tell the immune system what to do and how we can control them’.

JDRF-funded researchers in Canada have for the first time reversed type 1 diabetes in mice using human embryonic stem cells.

The team, led by Dr Timothy Kieffer, directed the stem cells most of the way towards becoming beta cells in the lab and the cells finally became mature beta cells once they were transplanted into mice.

Dr Kieffer turned stem cells into pancreatic progenitor cells which are the type of cell that becomes a beta cell and then transplanted them into mice. The environment around the pancreas of each mouse helped to turn the cells from pancreatic progenitor cells to beta cells and by five months after the transplant, the mice were producing their own insulin in response to glucose.

However, the team also needed to give the mice strong drugs to suppress their immune systems so that they would not reject the transplant.  This can be problematic for humans as it causes significant side effects, including reducing ability to fight off infections.

In type 1 diabetes, the cells in the immune system destroy the insulin producing beta cells in the pancreas. Replacing or regenerating beta cells could give people with type 1 the ability to produce their own insulin.

However, beta cell therapies are unlikely to be a cure by themselves and will need to go hand in hand with better immune therapies that will selectively stop the part of the immune system that attacks beta cells.  In the future, this could prevent some of the side effects of beta cell transplants.

Sarah Johnson, Director of Policy and Communications  said ‘This is a step forward in our aim to be able to restore insulin production in people with type 1.  There is a lot more work to be done to build on this promising research, which is only made possible by the generosity of JDRF supporters worldwide,'

Find out more about how to support research to cure, treat and prevent type 1 diabetes.

JDRF-funded researchers at Oregon Health and Science University have discovered a way to keep liquid glucagon stable so that it could be used in diabetes pumps.

The research which was led by Dr W Kenneth Ward was presented at the American Diabetes Association’s (ADA) annual scientific meeting this week. Dr Ward and his team found that reducing the level of acid in the glucagon compound meant that it could be kept as a liquid for longer periods of time. At the moment, glucagon cannot be stored as a liquid and is kept as a powder which, when added to liquid needs to be used immediately.

This research could broaden the use of glucagon to treat hypoglycaemia and is an important step towards the development of a multi-hormone, automated artificial pancreas. Future generation artificial pancreas systems could act just like the body and be able to release glucagon as well as insulin to keep a tighter control on blood glucose levels.

Glucagon is a hormone that raises blood sugar levels and works together with insulin to fine tune blood glucose levels. Previous research has shown that insulin treatment together with glucagon reduces hypoglycaemia. 

Rachel Connor, Head of Research Communication at JDRF said, ‘JDRF are committed to developing the next generation multi-hormone artificial pancreas and for this we need stable liquid glucagon that can be used in a pump. Dr Ward’s research is an exciting step towards this goal.’

Read about more JDRF-funded research that has been presented this week at the ADA meeting on the JDRF US site