Our immune system is the human body’s army that defends our body from invaders, such as viruses, bacteria, and other infections. When a nation’s army revolts against its own government, the nation faces a crisis. A coup results or there is an attempt to quash the revolt.
When you translate this scenario to our body, the revolt is the equivalent of an autoimmune condition. When a coup occurs, our body is actually succumbing to the disease caused by the attack of the infectious agents.
In the case of type 1 diabetes, it is not clear how exactly it arises. Today, research is trying to unravel the complex nature of type 1 diabetes. One such attempt by researchers at Cardiff University shows the answer may lie in the immune system’s killer T cells.
The experiments are preliminary in nature since they were performed in a laboratory to understand how well the immune system’s T cells react with different agents, including pathogens.
Like a lock and key mechanism, killer T cells recognize foreign agents in the body. They trap these agents by binding to their surfaces.
The research team noted the killer T cells had the capacity to react to 7 different protein molecules, including a bacterial protein molecule.
To date, it was assumed that T cells would only trap foreign agents. Only when there is any irregularity in the cell, would they start attacking the body’s cells.
However, the research team showed through their experiments that the T-cells could actually recognize a wide range of molecules.
“And binding a pathogen (e.g. germs) could trigger these T cells to begin attacking the body’s own cells. This self-inflicted attack may be the cause for the development of type 1 diabetes.”
The results, though preliminary, could initiate further research in this area to detect the potential onset of type 1 diabetes.
