Individuals suffering from type 1 diabetes battle against the destruction of some cells in the pancreas. According to the studies, these pancreatic cells are often mistaken as foreign invaders. Good news is, one of the unfortunate triggers that cause this destruction has already been discovered by a team of researchers in Switzerland.

The cells that suffer the unfortunate destruction are called beta cells. Beta cells are produced normally in packages of proteins called exosomes. The recent study discovered that in cases of stressful events, exosomes are filled with chemicals that serve as warning signals that attract immune cells.

"When beta cells are subjected to stress, the exosomes are released at higher levels and now contain proteins that signal danger to alert the immune system," according to author Steinunn Baekkeskov. Baekkeskov is also a biochemist at the Swiss Federal Institute of Technology in Lausanne, Switzerland.

These latest information can provide a way to silence the wayward immune system and prevent development of early stages of type 1 diabetes, according to the researchers.

Mysterious Target

Beta cells are responsible for releasing insulin. Insulin is a hormone that aids the body in processing sugar in the bloodstream. People suffering from diabetes 1 have depleted beta cells. Therefore, they must inject insulin in their bodies, otherwise, they may die. Type 1 diabetes patients need to monitor their blood sugar levels constantly and need to maintain with doses of insulin each day to regulate their blood sugar.

Despite the insulin treatment, there is risk for people with inconsistent blood sugar levels. Blood sugar levels that peaks and drops may pose a serious health risk and cause complications to the kidney, heart and nerves.

An ongoing study allowed for a group of researchers to monitor family members of people with type 1 diabetes-this members also have a high risk of developing diabetes as well. The scientists found that the stress experienced by the immune system begins even before the person exhibits any symptoms.

At the onset of the disease, the individual may still have elevated levels of antibodies that can bind to pancreatic proteins that are found in beta cells. Once a person proves positive for 2 or more antibodies to these proteins, it will certainly result to the development of the disease in the long run- this remains true even if the person does not exhibit symptoms for years, confirmed by a 2015 study in the Diabetes Care journal.

The findings of the research allowed researchers to gain better understanding in planning an earlier intervention to prevent shutting off immune attack in individuals with antibodies and a avoid the death of more beta cells, according to Baekkeskov.

"Antibody-positive individuals, who have not yet developed clinical disease, are candidates for immune preventive therapy to block beta-cell destruction and prevent the development of type 1 diabetes," Baekkeskov added.

Seeds Of Destruction

The researchers admitted that they are still in the process of understanding how the beta-cell proteins initially behave in their encounter with cells of the immune system causing the autoimmune trigger.

Baekkeskov and her colleagues studied the exosomes of both human and rat beta cells. The group discovered that the exosomes carries the beta-cell proteins detected by the antibodies. Additionally, the exosomes are more inclined to attract immune cells and activate them consquently, according to Baekkeskov.

The exosomes were also attached with chaperone proteins or special molecules that that take newly made proteins and aid in the folding and travelling through the cell to the final destination, Baekkeskov added.

The chaperone proteins were not benign as they acted as a warning of danger to the immune system. Following this reaction the molecules of the immune system alert the molecules and interpret the reaction as danger, the researchers further hypothesized as published in the Nov. 21 issue of the Diabetes journal.

These findings promises a new way to potentially reprogram the immune system by finding a way to engineer an exosome mimic with chemical signals that can attract the beta-killing immune cells and block or kill them.