Before going into the details of this discovery, it would be a good idea to go back to the basics and understand what diabetes type 1 actually is. This form of diabetes is a condition where the immune cells attack the beta cells, the active insulin producing cells within the pancreas. Most research being carried out on diabetes is focused on finding a solution to the problem, rather than looking deeper into what causes diabetes in the first place.

The key to a cure lies in searching for a cause. That is precisely how, a Melbourne researcher, Professor Len Harrison and his team has managed to take a big leap in the direction of understanding diabetes 1. In an exciting turn of events, Professor Len has found that the immune protein CD52 can potentially halt the progression of type 1 diabetes, by preventing the destruction of beta cells, the cells that produce insulin. In other words, CD52 acts as an immune suppressant, regulating the activity of the body’s immune responses. Confused? Well! In simple terms, your immune system is your body’s regulatory mechanism, protecting you from any agent that is causing damage to the system-kind of like a regulatory police of the body. There has to be some mechanism to keep these regulatory cells in line as well, to prevent them from overstepping their boundaries-something that happens in diabetes type 1. That’s the job of CD52, and a greater concentration of cells that release or have CD52 prevents the immune cells from exceeding their boundaries, preventing autoimmune diseases.

Currently, the team is working to completely halt diabetes in animals. Eventually, the research will be translated into human beings, and the way things are going, positive results are expected from the research. What’s exciting about the team’s research is the possibility that CD52 could help completely eradicate many of the autoimmune conditions that we’re currently struggling to cope with-not just diabetes. Let’s just say it’s a step in the right direction, if not a part of the solution.

Read about Dr. Len’s research in more detail here…