Lots of research news these days … here are a few exciting ones!
MGH study shows vaccine could permanently reverse type 1 diabetes, as reported in the Boston Business Journal, 10 June 2017. Researchers from Massachusetts General Hospital have discovered that a vaccine could permanently reverse the disease.
Dr. Denise Faustman, director of the Massachusetts General Hospital immunobiology laboratory and principal investigator of the trial, said interim results show that unlike other vaccines that irritate white blood cells to prompt an immune response, the BCG vaccine affects white blood cells at the genetic level, regulating which genes are expressed and which are not. The body consequently stops producing the abnormal white blood cells responsible for the autoimmune disease, suggesting that the vaccine could permanently reverse type 1 diabetes.
“The vaccine actually resets your genes to restore normality,” Faustman said in an interview. “What it is showing is it’s not merely the vaccine you’re being given and it causes inflammation or an immune response. It’s actually working at the most basic DNA level to normalize expression of genes related to this abnormal immune response.”
JDRF Invests in TetraGenetics’ Innovative Approach to Type 1 Diabetes Prevention was highlighted in ASweetLife.com, June 2017.
A unique scientific approach to preventing, treating and, perhaps one day, curing type 1 diabetes is being coupled with JDRF’s equally innovative approach to funding such studies in a new partnership that might move the promise of a preventive therapy and improved treatment for the condition closer to reality.
The big picture view is that type 1 diabetes is an autoimmune disease, meaning that the body’s own immune system attacks insulin-producing beta cells in the pancreas, killing them and causing the condition.
Lean in closer and squint and you’ll discover something called “effector memory T-cells” and a component of those cells called Kv1.3 ion channel proteins. Effector memory T-cells are the specific immune cells that kill insulin-producing beta cells. “Ion channels control many functions in the body and Kv1.3 controls activation of effector memory T-cells,” Clark says.
“These effector memory T-cells are associated with the autoimmune cascade that causes type 1 diabetes and they contain high levels of the Kv1.3 ion channel proteins,” according to a news release from TetraGenetics and the JDRF.
Brit scientist could be about to CURE multiple sclerosis and provide hope for millions, as reported in the Science section of the Mirror UK, 10 June 2017
Dr Su Metcalfe and her team at LIFNano believe they have found the cure for the devastating condition, multiple sclerosis. More than 2.3million people globally are affected by the debilitating condition and symptoms include blindness and muscle weakness.
Dr. Metcalfe said: “I was looking to see what controls the immune response and stops it auto-attacking us,” she explains.
“I discovered a small binary switch, controlled by a LIF, which regulates inside the immune cell itself. LIF is able to control the cell to ensure it doesn’t attack your own body but then releases the attack when needed.
But the breakthrough wasn’t over then, as the LIF could only survive outside the cell for 20 minutes before being broken down by the body, meaning there was not enough time to deploy it in a therapy. And this is where the technology, in the form of nano-particles, comes in.
Dr Metcalfe said: “They are made from the same material as soluble stitches, so they’re compatible with the body and they slowly dissolve,” says Su.
“MS is our key driver at the moment, but it’s going to be leading through to other major auto-immune disease areas,” she adds. “Psoriasis is high up on our list, and diabetes is another. Downstream there are all the dementias, because a LIF is a major health factor for the brain.
Novel tissue-engineered islet transplant achieves insulin independence in type 1 diabetes, published by ScienceDaily, 11 May 2017, from the May 11 issue of the New England Journal of Medicine.
Scientists from the Diabetes Research Institute (DRI) at the University of Miami Miller School of Medicine have produced the first clinical results demonstrating that pancreatic islet cells transplanted within a tissue-engineered platform can successfully engraft and achieve insulin independence in type 1 diabetes.
“The objective of testing this novel tissue-engineered platform is to initially determine that insulin-producing cells can function in this new site, and subsequently introduce additional technologies towards our ultimate goal to replace the pancreatic endocrine function lost in type 1 diabetes without the need for anti-rejection drugs, what we call the DRI BioHub,” explains Camillo Ricordi, M.D., director of the DRI and the Stacy Joy Goodman Professor of Surgery, Distinguished Professor of Medicine, Professor of Biomedical Engineering, Microbiology and Immunology at the University of Miami Miller School. Dr. Ricordi also serves as director of the DRI’s Cell Transplant Center.
Fluorescence microscopy of islets in the omentum transplanted within the biologic scaffold. In red (insulin staining) and blue (DAPI nuclear staining). Credit: Diabetes Research Institute/University of Miami Miller School of Medicine
Glucagon-Blocking Drug Reduces Need for Insulin and Improves Blood Glucose Levels for Patients with Type 1 Diabetes, in news provided by the American Diabetes Association, 13 June 2017
A single dose of the glucagon-blocking drug REMD-477 can substantially reduce the amount of insulin needed and improve glucose levels without increasing hypoglycemia (low blood glucose levels) in patients with type 1 diabetes, according to the study, “REMD-477, a Human Glucagon Receptor (GCGR) Antibody, Reduces Daily Insulin Requirements and Improves Glycemic Control in People with Type 1 Diabetes (T1D),”
Glucagon is a hormone produced by the pancreas that raises blood glucose and works together with insulin, which has the opposite effect, to tightly regulate blood glucose concentrations. In individuals with diabetes, glucagon effects may not be appropriately balanced by insulin, resulting in elevated blood glucose.
“Our study strongly supports the long-held theory that blocking glucagon may have a significant clinical impact on care for people with type 1 diabetes by improving glucose levels and lowering insulin doses,” said Jeremy Pettus, MD, assistant professor of medicine in the endocrinology department at the University of California, San Diego. “We expected that the drug [REMD-477] would have an effect, yet the degree to which the drug reduced the need for insulin and improved patients’ blood sugar levels without increasing hypoglycemia events was a surprise.”