Researchers in Switzerland may have identified the “attack” signal in type 1 diabetes.
Researchers in Switzerland have identified the long-sought “attack” signal in type 1 diabetes.
According to a new study, certain cells called beta cells in the pancreas are usually targeted in people with type 1 diabetes because it mistakes them for foreign invaders, but researchers may be on the way to stave off the disease if caught early enough.
The cells that are destroyed normally produce certain proteins in packages called exosomes and researchers from the Swiss Federal Institute of Technology in Lausanne, Switzerland, found that when the cells are in trouble, such as after an infection or other stressful event, these packages are decorated with chemical warning signals that may act as homing beacons that lure immune cells.
With the new findings, scientists could provide a means to shut off the wayward immune system and prevent the development of the disease in people who are at very early stages, according to an article in Live Science.
Beta cells normally release insulin, which helps body cells take in sugar from the bloodstream.
However, for people with type 1 diabetes whose beta cells are destroyed, they must inject insulin into their bodies and also must constantly monitor their blood sugar and take several doses of insulin each day to regulate their blood sugar.
Despite ongoing treatment, blood sugar levels often run too high and too low in people with the condition, increasing the risk of complications like kidney failure, heart disease and nerve damage.
Scientists have often monitored the family members of people with type 1 diabetes and found evidence that the autoimmune attack begins before symptoms are visible.
Scientists have discovered that early on in the course of the disease people may have high levels of certain antibodies that bind to pancreatic proteins found in the beta cells.
According to a 2015 study in Diabetes Care, when a person tests positive for two or more antibodies to these proteins it virtually guarantees that they will eventually develop the disease.
Study author Steinunn Baekkeskov, a biochemist at the Swiss Federal Institute of Technology, said the findings raised hopes of intervening early to shut off the immune attack in people with antibodies before too many beta cells are destroyed.
Baekkeskov led a team that analyzed the exosomes from both human and rat beta cells and found that the exosomes carried the beta-cell proteins recognized by the antibodies. The exosomes also attracted immune cells and activated them, according to the Live Science article.
Also when the cells were under stress, the exosomes were decorated with chaperone proteins—special molecules that take newly made proteins and help them fold or travel through the cells to their final destination.
However, these chaperone proteins were not benign and signaled danger to the immune system.
One possible theory is that inflammation, including as the response to an infection or other assault, stresses the beta cells and causes them to release exosomes marked with these warning signals. When that happens the immune system launches an unrelenting assault and is very difficult to shut off.
The findings may lead to a new way to reprogram the immune system by engineering an exosome mimic covered with chemical signals that can lure the beta-killing immune cells to them and block or kill them.
