Scientists discovered that the absence of two proteins, Puma Bin, causes immune cells to attack organs meant to be protected. This can lead to autoimmune disorders such as type-1 diabetes and arthritis.
Daniel Gray and his colleagues at the Walter and Eliza Hall Institute’s Molecular Genetics of Cancer division and University of Ballarat have discovered that this pair of proteins molecules work together in order to kill’self reactive’ immune cells, which are programmed to attack their own organs.
Journal “Immunity”, reports that autoimmunity diseases such as type-1 diabetic, rheumatoid arthritis, inflammatory intestinal disease, and multiple sclerosis develop when immune cells attack the body’s cells, destroying vital organs or body structures. Puma, Bim and other BH3-only proteins cause cells to die through a process known as apoptosis. Eliza Hall said that defects in apoptosis protein have been linked to a variety of human diseases including cancer and neurodegenerative disorder.
Gray explained that the body can protect itself from autoimmune diseases by forcing self-reactive cells to die while they are developing. He said that if any self-reactive cell reaches maturity, the body has a secondary safeguard to switch these potentially harmful cells into a state of inactivity, preventing them from creating autoimmune diseases. Gray now collaborates with researchers who identified human genes linked to autoimmune conditions. Gray explained that “we now know self-reactive cells death is an important protective factor against autoimmunity.” The next step in our research is to determine whether defects in cell death processes work together with other factors to trigger human autoimmune diseases.
