Proteins offer protection from type 1 diabetes
Daniel Gray and colleagues from the Walter and Eliza Hall Institute's Molecular Genetics of Cancer division and the University of Ballarat in Australia discovered that the protein molecules called Puma and Bim collaborate to kill 'self-reactive' immune cells.
These turn on the body's own cells and damage or destroy vital organs or structures, which leads to the development of autoimmune conditions such as type 1 diabetes, multiple sclerosis and rehumatoid arthritis.
Puma and Bim are so-called `BH3-only` proteins that kill these cells through a process called apoptosis or self-death. Previous studies have linked defects in apoptosis proteins to a number of human diseases, including cancer and neurodegenerative disorders.
One way the body protects itself against autoimmune disease is by forcing most self-reactive immune cells to die during their development, Gray explained.
"If any self-reactive cells manage to reach maturity, the body normally has a second safeguard of switching these potentially dangerous cells into an inactive state, preventing them from causing autoimmune disease," he said.
"We were able to use this discovery to show that the death of self-reactive immune cells is indeed an important protection against autoimmunity."
The scientist is now working with researchers who have identified human gene defects linked to the development of autoimmune conditions.
"The next stage of our work is to discover whether defects in the cell death process cooperate with other factors to cause human autoimmune disease," Gray added.
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