New medical trials have started at the National Institute for Health Research Biomedical Research Centre at Guy’s and St Thomas’. The aim of these ground-breaking trials is to stop the progression of Type 1 Diabetes in people who have recently been diagnosed with the disease but still have some functioning beta cells remaining. The researchers are testing their new immunotherapy, which targets regulatory T cells by exposing them to fragments of beta cells’ proteins. If the autoimmune process responsible for destroying cells is stopped, then the continual loss of beta cells will in turn be halted. In fact, this immunotherapy has already been put to the test: it has helped 27 people in the UK to slow the progression of their diabetes so far, and, thankfully, larger trials are in the pipeline.
Source: BBC News Health, 9th August 2017
Viacyte, a company based in California, USA, has come up with an implant whose sole aim is to replace islet cells that are lost as a result of T1D.
These vital islet cells are replaced by a derivative of stem cells called Progenitor cells, which are encapsulated in an implant the size of a credit card. After being subcutaneously implanted, the Progenitor cells mature into islet cells that produce insulin, meaning that blood glucose levels can be controlled without regular injections.
Despite the fact that there are several disadvantages to this new approach, namely, the inescapable need for immunosuppressants, the unaddressed autoimmunity component of the disease and the size of the device, the results of three experimental trials on human volunteers are highly anticipated.
Sources: New Scientist No3138, 12 August 2017;
Viacyte, Inc. website; located at http://viacyte.com/.
Beta cells in type 1 diabetics aren’t exactly very abundant, and transplanting replacement cells into the pancreas is laborious, expensive and, worst of all, temporary. That’s why gene transfer, which coaxes non-beta cells in the pancreas into making insulin, promises to be an ideal method of curing diabetes.
This method of gene transfer, called cellular networking, integration and processing, works by sneaking certain genes into the pancreas using a virus. According to Dr. Ralph DeFronzo from the University of Texas, the co-author of the study which used this technique to counter diabetes mellitus in mice, these edited pancreatic cells acted “basically just like beta cells” by secreting insulin “only in response to glucose”.
What’s more, the cells’ ability to produce insulin was maintained in the long term, and didn’t result in any side effects. However, as with all animal studies, this has yet to be replicated in humans, or even larger animals with physiology that more closely matches that of humans: the researchers hope to reach human clinical trials within the next 3 years, but only after testing their technique in large animal models.
While this approach shows potential just like many others mentioned on this blog, it’s a long way from being implemented in reality, and whether it will even work in humans is another questions. This particular issue was raised in the comments section of the quoted article: one diabetic, who said he’s had diabetes since 1975, pointed out that he has seen a vast array of cures that have worked on diabetic mice, only for them to seemingly disappear like a mirage in a seemingly endless desert.
Source: Type 1 diabetes cured in mice using gene therapy, by Honor Whiteman.
The non-invasive testing of blood sugar levels have seen much development and breakthroughs in the past decades thanks to much research aiming to reduce diabetics’ dependence on finger-pricking, which is not only wasteful, but also slightly painful. Therefore it is very encouraging to hear about a new development from scientists at the Seoul National University, who have developed a flexible sensor patch to detect sugar levels in sweat. Testing sweat is more technically challenging than conventional methods of testing blood sugar levels due to the low concentration of sugar in sweat when compared to blood, while several other properties of sweat that complicate this process have to also be accounted for. However, the South Korean researchers have overcome these issues, and are also now working on another patch to deliver insulin through an array of tiny needles. We’ll be looking forward to new developments.
Source: BBC News website, 9/3/17
The Queen Alexandra Hospital in Cosham, UK, may seem an unlikely place to produce a Marvel-style comic. However, it was Dr Partha Kar, in collaboration with Dr Mayank Patel and some of their patients, as well as publishing company Revolve Comics, who came up with Type1:Origin, a comic strip about the extraordinary life of an initially very ordinary teenage boy who struggles with the intrusion of diabetes in his life (also note the sneaky Marvel reference in the title).
Moreover, Marvel has made attempts in the past to inform readers about diabetes through the medium of the comic book. Indeed, their prior creation, ‘Iron Man: Early Warnings’ doesn’t make a distinction between T1 and T2, thus potentially misinforming their audience. However, the comic Type1:Origin is, in my opinion, a good attempt to introduce newly diagnosed teens to their condition without the ambiguity of previous comics.
Sources: portsmouth.co.uk , revolvecomics.com , marvel.com
Andrea Graham, an evolutionary biologist, and her colleagues at Princeton University, have found that people with high levels of “self-reactive” antibodies (implicated in autoimmune diseases’ development) were less likely to have a type of chronic viral infection and were more likely to live longer.
Some scientists believe that these self-reactive antibodies might clear dying cells and other debris from the body, and even play a role in watching for cancer cells.
It seems that evolution produced autoimmunity to bring advantages to humans (Aaron Blackwell, an evolutionary anthropologist at the University of California, Santa Barbara, concurs); unfortunately, as T1D and other autoimmune disease sufferers know, evolution sometimes misfires. It really might be a case of ‘too much of a good thing’.
Source: New Scientist 29 July 2016
Although stem cells have been shown to have great potential in curing autoimmune diseases such as type 1 diabetes (see my first post about stem cell treatments for more information), there is one key issue that prevents this cure from being viable: 1 in 5 patients die from the process of stripping the body of the part of the immune system that is ill.
However, this will no longer be the case with Stanford University’s novel discovery of antibodies that attach to malfunctioning cells (usually blood stem cells) and tag these cells for removal by macrophages, whose role is to devour any potentially toxic substances in the body. This consequently ensures that the transplanted stem cells can be introduced safely into the body and can take up residence in the bone marrow, thus creating a new immune system with close to zero risk of death.
This process will hopefully replace radiotherapy and chemotherapy, which are currently used in this process to strip the body of the malfunctioning immune system and often result in several toxic side effects such as damage to the brain, liver and reproductive organs.
What makes this treatment even more useful is that it can be used with many autoimmune diseases such as multiple sclerosis in addition to being one way of removing the need for immunosuppressant drugs after organ transplants in order to prevent the immune system rejecting donor organs.
Source: Hope of cure for arthritis, MS and diabetes as Stanford makes stem cell transplants safe from telegraph.co.uk, by Sarah Knapton