White Blood Cells May Cause Diabetes with “Friendly Fire” Accident
Scientists have made a step forward in understanding how type 1 diabetes develops after discovering that killer T-cells may attack the insulin-making cells in the pancreas. These ferocious lymphocytes, programmed to attack and destroy invading bacteria, seem to be at the root of type 1 diabetes, which is known to be caused by an autoimmune response. The researchers say the discovery brings closer the day when medical science will be able to prevent or cure the disease.
Type 1 diabetes accounts for about 10% of diabetes cases, and typically is diagnosed before the age of 20. It may even develop in tiny babies, and is believed to have a link to family genetics.
When we eat, sugars from the food enter our bloodstream quite quickly, and our body responds by sending out insulin, a hormone produced in the pancreas. This chemical messenger tells the body’s cells to take in the glucose and store it. In this way, blood sugar levels fall again and the cells have the benefit of the glucose for their own energy needs.
However, in a type 1 diabetic the beta cells that actually make the insulin are damaged or destroyed by the immune system. The diabetic will have to monitor his blood sugar levels and have insulin injections for the rest of his life to stay healthy. Like type 2 diabetes, type 1 is associated with serious side effects such as heart and kidney failure, strokes, blindness and nerve damage if the blood sugar levels are not well controlled. Nerve damage can lead to gangrene and deformities, and sometimes feet and other extremities may have to be amputated, one of the most feared outcomes in the disease. A diabetic may also be more prone to infections because his immune system is compromised.
The British scientists, including T-cell expert Professor Andy Sewell fromCardiffUniversityand a team of experts in diabetes isolated a T-cell from a diabetic person and observed the interaction that resulted in beta cells being attacked. The T-cell, a large spherical lymphocyte, or white blood cell, programmed to attack infection-causing bacteria, seems to attack the beta cells by accident in a kind of biological “friendly fire”.
The team reported that seeing how the T-cells make their first contact with the beta cells has increased their understanding of the process by which diabetes is caused. The study could potentially put medical science in a better position to identify patients who are likely to get the disease or even to prevent the series of events that lead to diabetes. Even in a person who has an increased likelihood of type 1 diabetes, perhaps because it runs in his family, the better understanding of the process could help doctors to halt it before too many beta cells have been lost. If beta cells were saved, the patient would still be able to manufacture insulin, possibly enough to function without any need for injections of the hormone. This would have obvious implications for diabetes patients, who are tied to a cycle of blood testing and injections in order to stay healthy.
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