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Displaying beta cells


Injection of millions: massive investment follows Dr Melton’s stunning stem cell research breakthrough for type 1 diabetes

You’d be forgiven for suspecting that things sometimes go a bit quiet after global headlines shout about a type 1 diabetes research breakthrough.

But JDRF’s Harvard hero Doug Melton, whose work turning stem cells into insulin-producing beta cells made worldwide news last October, has announced two massive new business collaborations designed to bring his research to fruition sooner.

The first, which has raised £30 million from several companies including Medtronic, will aim to develop beta cells that can be transplanted into the body.  In type 1 diabetes, the immune system destroys these insulin-producing beta cells, so a procedure that could give them back to people could mean an end to insulin injections and blood glucose testing. It’s why we, too, are funding Dr Melton as part of our encapsulation research.

The second collaboration, a partnership with pharmaceutical company AstraZeneca, will see researchers study the beta cells to learn more about their biology, giving us new insights into how type 1 diabetes develops. The cells will also be tested against many of the drugs developed by AstraZeneca, to see if any could be used to cure or even prevent the condition.

Until now, beta cell research in both of these fields had been hindered by a lack of donated pancreases, and by the more lengthy process normally used to grow the cells in the lab. Work by Melton, and by other JDRF-funded researchers such as Timothy Kieffer, should therefore help speed up the process of turning lab-based discoveries into treatments for people with type 1 diabetes.

Dr Clare McVicker, Director of Research Advocacy at JDRF in the UK, said: ‘A £30m investment is a huge stamp of approval for Dr Melton’s research. Business only backs scientific developments when it sees true potential – and this could change type 1 diabetes treatment globally.’

Read more about Dr Melton here.


Could a blood pressure drug help beta cells survive? People with type 1 diabetes will soon help researchers find out

A new clinical trial is due to begin shortly, testing whether a commonly used blood pressure drug, verapamil, can help remaining insulin-producing beta cells survive in people newly diagnosed with type 1 diabetes.

The trial is the result of many years of laboratory research – much of it supported by JDRF – gaining insights into how beta cells work in people with diabetes. The research team, led by Dr Anath Shalev at the University of Alabama at Birmingham, have found that when a person develops diabetes and their blood glucose levels rise, their body starts overproducing a protein called TXNIP. Research has shown that an excess of TXNIP in beta cells triggers a process of cell death, which of course makes it even harder for the body to regulate blood glucose effectively.

The research team then started to search for drugs that could help reduce TXNIP in beta cells. And they found that verapamil, which is widely used in the treatment of high blood pressure, irregular heartbeat and migraine headaches, fitted the job description.

Working with mice with diabetes, the team found that the drug was very effective – not just halting beta cell decline, but actually restoring the mice’s ability to make their own insulin. The team have planned the new clinical trial to find out if the drug can have a similar effect in people with type 1.

There is no current treatment for diabetes that targets beta cell growth and development in this way, so if the results of this trial are positive, it might establish a completely new treatment paradigm for type 1 diabetes.

This trial will be a stepping stone to see if the approach can work. In the best case scenario, this trial would see beta cell mass completely restored in all the people taking the drug in the study. This is unlikely – but a more subtle effect would still be very beneficial explains Dr Shalev: 'We know from previous large clinical studies that even a small amount of the patient’s own remaining beta cell mass has major beneficial outcomes and reduces complications. That’s probably because even a little bit of our body’s own beta cells can respond much more adequately to very fine fluctuations in our blood sugar — much more than we can ever do with injections or even sophisticated insulin pumps.'

The announcement of this clinical trial goes to show how important detailed ‘basic science’ studies in the lab can be – a thorough understanding of beta cells biology is what has made this trial possible. JDRF is proud to have supported the lab science that has got us to this point, and to be providing the funds for the clinical trial that will test whether the approach can work in people.

Karen Addington, Chief Executive of JDRF in the UK commented 'Repurposing existing drugs to address the fundamental challenges of type 1 diabetes – in this case the loss of the beta cells which make insulin - is a smart approach. Years of work in the lab to understand how beta cells work has allowed scientists to identify a target and then search out existing drugs that act on it. This trial will now allow us to see if the positive findings in animals can translate into humans. We eagerly await the results.’


Dr. Melton – the Harvard hero behind today’s type 1 diabetes stem cell breakthrough – thanks JDRF

You’ve seen the news today. Harvard stem cell researchers have announced a ‘giant leap forward’ in the quest to find a truly effective treatment for type 1 diabetes. 

With human embryonic stem cells as a starting point, the scientists are for the first time able to produce – in massive quantities – human insulin-producing beta cells equivalent in almost every way to normally functioning beta cells. It’s not yet a cure. But it’s big news.

Now meet the man who led this breakthrough.

Dr. Doug Melton is Co-scientific Director of the Harvard Stem Cell Institute. When his then-infant son Sam was diagnosed with type 1 diabetes 23 years ago, he dedicated his career to finding a cure for the condition. His daughter, Emma, also lives with type 1 diabetes.

The 61-year-old Cambridge graduate has previously been listed among TIME magazine’s 100 most influential people in the world. Jose Oberholtzer, Associate Professor of Surgery, Endocrinology and Diabetes and Bioengineering at the University of Illinois said: “Doug Melton has put in a life-time of hard work in finding a way of generating human islet cells in vitro. He made it.”

When he told his son and daughter about his breakthrough, they were surprisingly calm. He said: “I think like all kids, they always assumed that if I said I’d do this, I’d do it.”

Melton is now beginning a US$4 million project with JDRF, for the next stage of development of these cells. Expressing gratitude to the charity and its supporters, Dr. Melton said: “their support has been, and continues to be essential.”


Molecule supports glucose removal without raising hypo risk

JDRF-funded researchers in Boston, USA, have developed a way to support insulin in removing glucose from the blood, without increasing a person’s risk of hypoglycaemia.

The chemical, known as a glucokinase activator, could also indirectly improve the survival rate of beta cells, and so could theoretically be used to treat both the causes and the symptoms of type 1 diabetes.

Glucokinase activators are so called because they support the work of molecule called glucokinase. This is produced by the body to help remove glucose from the blood, converting it into a similar chemical that can be either stored or broken down. Because of this, glucokinase activators have been investigated in people with type 2 as a complement to insulin in lowering glucose levels.

In addition, some studies have suggested that the presence of glucokinase supports healthy beta cell growth, which would be beneficial to people with type 1. This would also require a glucokinase activator, since in the body glucokinase production is encouraged by rising insulin levels – something that people with type 1 lack since they no longer produce their own insulin.

However, previous attempts at formulating glucokinase treatments have focused on changing the shape of the glucokinase molecule to make it better at interacting with glucose. This is useful when glucose levels are high, as the removal can happen more quickly, but when glucose levels fall, this increased ability to react runs the risk of causing hypoglycaemia, since unmodified glucokinase would normally stop working below a certain level.

The research team, led by Drs Loren Walensky and Nika Danial, created a new glucokinase activator that drives glucokinase to remove glucose more efficiently, but stop once levels fall to normal – at the point when it naturally stops working.

This would allow it to work without increasing the person’s risk of hypoglycaemia.

Although the research is currently at an early stage – in pre-clinical lab studies – the investigators suggest the molecule could eventually be used alongside insulin to help manage glucose levels. They predict that this will be especially useful for people with type 2, given the lower levels of glucokinase found in people with type 1, but say that ‘improvement of both beta cell function and mass through increased glucokinase activity may well expand the potential utility of synthetic glucokinase activators beyond [type 2] to restoration and maintenance of functional beta cell mass for the treatment of type 1 diabetes.’

The research was published in the journal Nature Structural & Molecular Biology.


Scientists grow insulin-producing cells using protein injections

Researchers in Belgium have successfully generated insulin-producing beta cells from other pancreatic cells in mice with type 1 diabetes. The mice were then able to control their own glucose levels without additional insulin.

The study, part-funded by JDRF, was published in the journal Nature Biotechnology.

In people living with type 1, the immune system attacks the beta cells of the pancreas, leaving the person unable to produce insulin. This means they cannot control their own blood sugar, and must rely on insulin injections to stay alive.

However, the other pancreatic cells remain functional, and reprogramming these to produce insulin is a potential pathway to treating the condition.

The researchers first simulated type 1 diabetes in the mice, then after five weeks gave some of these mice a course of proteins that have been known to stimulate beta cell growth in the lab.

The treated mice subsequently began producing insulin, and their blood glucose levels fell to match those of mice with functioning beta cells. The other mice continued to experience high blood glucose levels.

By tracing the genetic origin of the newly grown beta cells, the researchers found that they were mostly derived from another type of pancreatic cell, called acinar cells. These normally help the pancreas secrete digestive juices, and are not involved in insulin production.

Dr Harry Heimberg, the study's Principal Investigator, from the University of Brussels Diabetes Research Centre, said: “Several characteristics make acinar cells ideal candidates for reprogramming to beta cells in the pancreas: they are the most abundant cell type, their microenvironment is identical to that of beta cells and they are not affected by diabetes."

This study provides hope for those living with type 1 diabetes, but more research will be necessary to see if the findings can help those living with the condition, as it is likely that the immune system would still attack any newly-formed beta cells.

Dr Heimberg added: "We hope that our model will contribute to the development of a robust and safe strategy for beta cell therapy in diabetes."

Karen Addington, Chief Executive of JDRF, said: “The results from this study are interesting, and certainly appear deserving of further exploration. Type 1 diabetes is a challenging and complex condition. But it will one day be cured. It's just a matter of time, money and excellent research."


New JDRF-funded research projects announced

Dr Parth Narendran at the University of Birmingham will test if there is a way of stopping the cells of the immune system that target beta cells from entering the pancreas in the first place. Preventing the immune attack from getting started is one of JDRF’s key priorities. As the cells of the immune system usually reside in the blood, they need to pass through the walls of the blood vessels to get to the pancreas in order to wreak havoc.

Dr Narendran and his team have found that a molecule called PEPITEM appears to block exactly this passage of the cells that target beta cells for destruction through the walls of the blood vessels. If this proof of concept study proves successful, this could present an exciting new opportunity for protecting insulin-producing cells from immune destruction – both in people at risk of developing type 1 and people already living with the condition.

Dr Tim Tree at King’s College London is looking at specific cells in the immune system that may offer protection against type 1. In this project he will investigate regulatory T cells, which are supposed to keep the immune system under control. Previous work has identified a group of these regulatory T cells that are specifically involved in controlling the body’s immune response to insulin-producing beta cells, and people with more of these so-called ‘ISIS’ regulatory T cells seem to have a higher level of protection against getting type 1.

This project will help us to understand more about ISIS regulatory T cells and find out what makes them special. That understanding will then help us to work out if there is a way we can harness the power of ISIS regulatory T cells in our quest to cure and prevent type 1 diabetes.

In a related project at King’s College London, Dr Els Henckaerts is going to use her team’s skills in stem cell biology to investigate whether she can grow new regulatory T cells capable of controlling the immune response against beta cells in her laboratory. If this proof-of-concept study yields decisive results, the cells created by the team could potentially be injected into people with, or at risk of, type 1 diabetes as a means to control the immune destruction of beta cells.

JDRF has committed over £430,000 to supporting these three projects: find out how you can help us to support them today.


Behind the Headlines: Research breakthrough as experts reverse diabetes in mice

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.


Beta cells grow up

JDRF-funded scientists at Harvard University have provided new insights into to how stem cells develop to become insulin-producing beta cells.

The team, lead by Professor Doug Melton, have identified a marker which allows them to distinguish mature beta cells (which can produce insulin) from immature beta cells (which cannot).  The study is published in this month’s issue of the prestigious journal Nature Biotechnology.

Many scientists are working on ways to turn stem cells into beta cells. So far, they have managed to turn stem cells into immature beta cells in the lab, that when transplanted into mice will become mature beta cells that release insulin in response to glucose.  Although this is excellent progress, transplanting immature beta cells into humans is not ideal as there is a chance that some of the immature beta cells may not develop as expected, and instead begin multiplying out of control, causing cancer. For this reason, scientists want to be able to make fully mature beta cells in the laboratory which would then be much more suitable for transplantation.

Professor Melton’s work takes us a step further towards making mature beta cells in the lab. They have identified a protein that is found in mature beta cells but not in immature non- insulin producing ones. The protein, called urocortin-3, can now be used as a marker of mature insulin producing cells and will help scientists identify mature beta cells more easily when testing out new  ways to make them from stem cells. 

Rachel Connor, Head of Research Communication at JDRF said ‘Stem cells provide exciting possibilities for studying type 1 diabetes and potentially treating the condition in the future. Professor Melton’s study helps us understand more about how beta cells develop and crucially, also provides a way to efficiently test if new techniques for making mature beta cells from stem cells are working effectively’.


Beta cells: divide and conquer?

JDRF- funded scientists at the University of Pittsburgh in America have uncovered a new way to grow human beta cells in the lab.

The team led by Professor Andrew Stewart, were able to get human beta cells to divide and make more cells. Not only that, but they then managed to stop the cells dividing again. The research was published in this month’s issue of the journal Diabetes.

The researchers added genes called cdk and cyclin d into the beta cells. These genes make the cells divide and are usually switched off in beta cells. To deliver these genes into the cells they used a virus that can get into cells easily. Once they had enough beta cells, they added a drug to the cells which switched off the virus and stopped the cells dividing.

In the body, beta cells divide very slowly or not at all so when the immune system attacks them, the cells are not replaced. Usually in type 1 diabetes there are a few beta cells remaining and if scientists could make these cells divide they could replace the cells destroyed by the immune system.

It is also difficult for scientists to study human beta cells in the lab because beta cells are in such short supply. So making more of them will allow scientists to do more research towards finding a cure for type 1.

Although these researchers had previously shown that they could make beta cells divide, this latest study shows that they have developed a way to stop the cells dividing as well. This is particularly useful because the genes they used to make the cells divide are not usually switched on in beta cells - so when they are dividing a lot they are not identical to the beta cells in the body. Switching these genes off again makes them more similar to ‘real world’ beta cells, which means any discoveries scientists make using these cells  are more likely to be applicable to beta cells in the body.

Rachel Connor, Head of Research Communication at JDRF, said ‘These are very interesting results because it is often difficult for scientists to get human beta cells to study. Growing beta cells in the laboratory that are as similar as possible to those in our bodies will help type 1 diabetes researchers to test their ideas and develop new ways of treating type 1 much more effectively.’


A killer link to type 1 diabetes

JDRF-funded researchers at Cardiff University have shown exactly how cells in the immune system attack the insulin producing beta cells causing type 1 diabetes for the first time.

The research team, led by Professor Andy Sewell were able to shed light on the way that a particular cell of the immune system, called killer T cells target beta cells for destruction. Their research was published today in the latest issue of the prestigious journal Nature Immunology.

Killer T cells in the pancreas are very difficult to study as it is not easy to separate them from other cells. Professor Sewell’s team have developed a completely new technique for separating these cells out from the crowd. Having isolated the killer T cells they were then able to ‘watch’ the attack on the beta cells, as you can see from the picture (the t-cells are red and the beta cells are green) This allowed them to examine exactly how the cells recognised one another in incredibly fine detail.

Killer T cells normally recognise viruses like the ‘flu’ virus in the body and destroy them. But Professor Sewell’s team have discovered that they attack beta cells in a slightly different way. This may be why the immune system’s usual safety checks that ensure healthy ‘self’ tissues are not attacked are unable to pick up and control this process in type 1 diabetes.

These findings are particularly important as how and why beta cells are destroyed is still unclear. A greater understanding of this mechanism will enable scientists to develop new drugs to halt the process - or even predict and prevent type 1 diabetes.

Rachel Connor, Head of Research Communication at JDRF said ‘We’re really excited to see the results of this work – this is the first time scientists have been able to study the fine detail of how killer T cells target insulin-producing cells in type 1 diabetes. Research like this will be fundamental to allowing scientists to develop new, specific treatments that can help people with type 1’.

Thanks to Susan Wong for providing the cells and Maja Wallberg for taking the pictures.


Behind the headlines: diabetes breakthrough raises hope of cure

You may have seen in the Daily Mirror this morning, a report that a new cure for diabetes may be on the way.

The article discussed a new research study which showed that it may be possible to ‘re-educate’ the immune system of people with type 1 diabetes, and halt the destruction of insulin producing beta-cells that causes type 1.

In the study, stem cells from umbilical cord blood were used to retrain cells in the immune system not to attack the pancreas. Immune cells were taken from the patient and grown together with stem cells from donor umbilical cord blood. The patients' own cells were then separated from the stem cells and returned back into their blood. Growing stem cells and immune cells together seems to help stop the immune cells attacking beta-cells when they are put back in the patient. The approach appears to show promise as the first patients tested were able to reduce the amount of insulin they needed after the treated immune cells were returned.

This exciting discovery is new innovative approach to treating diabetes and JDRF is very pleased to have been involved in funding this research.

However, this was a small clinical trial which involved only 15 people and although the results are exciting, it is still early days for this treatment. The main aim of the trial was to test the safety of the treatment in people with type 1. As the trial showed that the treatment is safe, the research team can now run a larger clinical trial to prove if it works.

The way in which the stem cells ‘educate’ the immune system is also still unclear and more research will need to be done to understand this process before the treatment is likely to be accepted in to clinical practice.

You can read the full article here


Pass the parcel

Could tiny packets of stem cells help people with type 1 diabetes to produce their own insulin again? JDRF has joined forces with Viacyte, a US based biotechnology company, and the California Institute for Regenerative Medicine (CIRM) to help answer this question.

The organisations have come together to conduct preclinical testing of a first-of-its-kind cell therapy for type 1. The potential treatment is an innovative combination of cells and a special ‘packaging’ material. One of the unusual things about the therapy is that the cells, derived from embryonic stem cells, are not mature when they are packaged – rather they are immature human pancreatic hormone cells.

Initial tests have shown that once implanted, within their protective packaging, these immature cells develop into mature hormone producing cells, including the vital insulin producing beta cells that are missing in people with type 1. Tests in rodents have shown that once mature, these packets of cells are capable of regulating blood glucose levels.

Existing cell therapies such as islet and pancreas transplantation have the potential to cure type 1 by restoring normal islet function in people with the condition. But because there is a huge shortage of pancreatic islets from organ donors, it is important to find a replenishable supply of functional insulin-producing cells. This product, by using stem cells rather than tissue form organ donors could overcome this hurdle. Furthermore, packaging the cells in a device that creates a physical barrier around the cells (a process called "encapsulation") has the potential to protect the transplanted cells from immune rejection, and may eliminate the need for chronic immunosuppressive drugs.

The three-year series of preclinical studies being co-funded by JDRF will help prepare the information necessary to apply for regulatory approvals to study the system for safety and efficacy in people with type 1 diabetes.

Rachel Connor, Head of Research Communication at JDRF said ‘JDRF is excited to be working with Viacyte and CIRM on this pioneering project. Encapsulation technologies and stem cell therapies have fantastic potential in treating type 1 diabetes, so this type of innovation could be a huge step forward for people living with the condition.’


Putting type 1 in the picture

Mrs Chunjing Wang, who works at Birmingham University, has won JDRF’s first ever scientific photography competition. Her image (left) was judged to be both interesting and strikingly beautiful.

The photograph was taken through a microscope, using special fluorescent ‘tags’ to show up different features of an islet of Langerhans being attacked by immune cells.

Blue shows the insulin-producing cells in the islet, while green shows the immune cells which are attacking it. The red dots show cells which are multiplying – as these are mainly seen in green cells this image shows the scale of the immune attack.

The photograph had to fight off strong competition from a wide variety of images from other scientists working on type 1 diabetes related projects up and down the country.

Chunjing has a medical degree and masters degree from China. She is currently studying for a PhD in Dr Lucy Walker’s laboratory. This group is working to understand what makes the immune system attack the insulin-producing cells in the pancreas leading to type 1 diabetes, with funding from JDRF and other organizations.

The prize for the winning photograph is a £500 travel bursary. Describing what this will mean to her, Chunjing said “I am delighted that my image has won this travel bursary. I will now have the opportunity to travel to a scientific meeting where I can present my research findings and also keep up to date with what other researchers are doing.”

Scientific meetings are vital for scientists to exchange ideas and learn from each other. However, it can be difficult for scientists at the start of their careers, like Mrs Wang, to attend these meetings. This means that they may miss out on early opportunities to interact with other more established scientists, and hear from people working in fields slightly outside their own.

JDRF will be using all of the images entered into the competition over the coming months, through our website and publications to illustrate and explain stories about our research.


Scientists discover molecules that control insulin production

Some of JDRF’s most exciting research is exploring how to regenerate the cells which no longer produce insulin in people with type 1 diabetes. By working together with the pharmaceutical company Roche, JDRF-funded scientists have announced two new discoveries; a protein that controls how insulin-producing beta cells grow in the pancreas, and a chemical that can encourage this growth.

The study, which was led by Dr Markus Stoffel, a professor at the Swiss Federal Institute of Technology in Zurich, builds on a discovery made just five years ago. Dr. Stoffel and his team first showed that a previously unknown protein, called Tmem27, is situated on the surface of insulin-producing beta cells in the pancreas. Through tests conducted on mice, they found that increasing the levels of Tmem27 on beta cells meant that the number of beta cells increased.

After screening possible molecules that might be destroying the Tmem27 protein in people who develop type 1, Dr. Stoffel and his team found the culprit: Bace2. This is an enzyme that, like Tmem27, also resides on the outer surface of the beta cell. The researchers found that mice lacking Bace2 had larger islets and that their beta cells were actually regenerating. 
Dr. Stoffel and his team next aimed to stop Bace2 from being active in an effort to control and promote the growth of beta cells. To do so, they teamed up with scientists at Roche who developed a chemical compound that could inhibit Bace2. When the scientists gave this compound to mice, they saw that it stopped Bace2 and stimulated the growth of new beta cells. Importantly, this means that Bace2 can control the Tmem27 protein, suggesting the potential for developing a Bace2 inhibitor as a new diabetes therapy. 
This is exciting research, and the findings mean there is potential for a drug to be developed that promotes the growth of beta cells in people with type 1. Visit the research section on our website, to find out more about JDRF beta cell research.


Stem cells remember how to make insulin

JDRF-funded researchers in Israel have found that stem cells made from beta cells in the pancreas of adults have a ‘memory’ that makes them better able to produce insulin than other types of stem cell.

The team from Tel Aviv University, led by Shimon Efrat, published their discovery in the July issue of the journal Cell Stem Cell.

Stem cells can be taken from either embryos or adults. Both types have the potential to turn into many different types of cell, including insulin-producing beta cells. However this latest study suggests that the source of the stem cells has more influence than previously thought. The genetic ‘memory’ of stem cells derived from the pancreas means the cells find it easier to turn into insulin-producing beta cells, making them a better option for treating for type 1 diabetes.

Scientists hope to be able to use these stem cells to grow new beta cells to replace those destroyed in people with type 1 diabetes. When coupled with therapies to prevent or block the immune system from attacking the newly introduced beta cells, this research offers a possible route to a cure for type 1. 

This project forms part of the JDRF research programme aiming to find ways to replace or regenerate insulin-producing beta cells in people with type 1 diabetes. You can read more here. 


Time for more T regulatory cells

A JDRF-funded clinical trial is recruiting volunteers in the US to test the safety and feasibility of using regulatory T cells as a therapy for type 1 diabetes.

T cells are an important part of your immune system and there are a number of different types. Killer T cells play a vital role in the autoimmune attack that causes type 1 diabetes. Normally, these cells are kept in check by regulatory T cells, but in someone with type 1 diabetes these two types of T cell are out of balance.

This Phase I trial, led by researchers at the University of California, San Francisco (UCSF), aims to redress the balance by increasing the numbers of regulatory T cells. To do this, the researchers will first take blood samples from each volunteer. They will then isolate their T cells before multiplying them 1000-fold in the laboratory before infusing them back into the volunteer’s body.

If successful, this could pave the way for a Phase II trial testing whether the addition of regulatory T cells is able to stabilise the destruction of insulin producing beta cells.

Professor Stephen Gitelman, one of the lead investigators of the study at UCSF said: "For all these years, we have been looking outside of the patient to fight the autoimmune response that leads to type 1 diabetes, but now the answer may lie within the patients themselves."


Type 1 researchers follow gut feeling

Type 1 diabetes is caused by a combination of genetic and as yet unknown environmental triggers. Scientists know that the environment in your gut can play a role in the development of type 1 diabetes. However, they are not sure what effect the gut has on the autoimmune attack that destroys insulin-producing beta cells.

Now a research project funded by JDRF, published this month in the journal Diabetes, has shed light on how changes in the intestine can affect autoimmunity elsewhere in the body. 

The research team, led by Marika Falcone at the Experimental Diabetes Unit, San Raffaele Scientific Institute, Milan, collected biopsies from the small intestines of 12 people with type 1 diabetes, and compared them with samples from 17 people without the condition. They then counted the various types of immune cell present in the samples from each group.

In the samples from people with type 1 diabetes, the researchers discovered a significant reduction in the numbers of certain intestinal T regulatory cells – responsible for protecting against the autoimmune attack that causes type 1 diabetes.

Crucially, they found that the mechanism that creates these T cells in the gut had been disrupted. The researchers believe that this shows that the immune system environment in the intestine (partly responsible for maintaining a supply of good bacteria) is also instrumental in protecting beta cells in the pancreas. Further research is now needed to determine whether the disrupted mechanism has a genetic or environmental cause. 


JDRF partners with Selecta Biosciences to develop possible vaccine for type 1 diabetes

JDRF has announced a new research collaboration to support the development of a vaccine which may help better treat and potentially prevent type 1 diabetes.

The partnership with Selecta Biosciences will see JDRF provide expertise and financial support, with the goal of applying Selecta’s vaccine technology toward the development of vaccines for type 1 diabetes.

Selecta is working on a type of therapy called an ‘antigen-specific tolerogenic vaccine’. This is designed to specifically target the parts of the immune system that cause type 1 diabetes, without damaging the rest of the immune system. In addition to its potential in preventing type 1 diabetes, this type of diabetes vaccine could have other benefits. For example, they could be used in conjunction with other therapies to preserve remaining beta cell function in individuals recently diagnosed with type 1 diabetes. It may also help with regeneration and replacement therapies, and be used to protect newly regenerated or transplanted insulin-producing beta cells in established type 1 diabetes

JDRFI Chief Scientific Officer said: “We believe vaccine research is one of the most promising approaches to prevent or halt the beta cell-specific autoimmunity in type 1 diabetes. And we are excited to be teaming up with Selecta to support the development of this next-generation of vaccine technology.”

The research collaboration agreement between JDRF and Selecta is part of JDRF's Industry Discovery and Development Partnership (IDDP) program. Through this, JDRF partners with pharmaceutical, biotechnology, and medical device companies to prioritise and speed the discovery, development, and delivery of therapies and devices for type 1 diabetes.


JDRF scientists identify key trigger for beta cell regeneration

JDRF-funded researchers have identified a key signal that prompts existing insulin-producing beta cells in the pancreas to form new beta cells in mice. This breakthrough may help researchers find new ways to increase the number of beta cells in a person with type 1 diabetes.

The study, led by Professor Yuval Dor from the Hebrew University of Jerusalem and published this week in top journal Cell Metabolism, shows that it is the process by which beta cells convert glucose into energy that controls beta cell regeneration.

Researcher Shay Porat said: ‘This means that the more work that beta cells are required to do, the more of themselves they make.’

The five year study used a combination of surgical, pharmacological and genetic research techniques to understand the way glucose is used in beta cells. An enzyme called glucokinase, which triggers the first step in converting glucose to energy, was found to be the trigger that causes the beta cells to replicate.

Because this study showed that regeneration depends on glucokinase levels, rather than glucose levels, researchers may be able to develop targeted drugs to trigger beta cell regeneration.

Dr Eleanor Kennedy, Head of Research Communication at JDRF said: ‘This novel research suggests that existing type 2 diabetes drugs that activate glucokinase could be investigated as a new target for the treatment of type 1 diabetes.’

Regeneration research is among the fastest-growing scientific areas supported by JDRF, aiming to protect and regenerate insulin-producing cells in the body. You can read more about this research on our website.

Read the full article here (subscription required).