According to Australian researchers, the death of your immune system cells is an important asset to your wellbeing, as it safeguards your wellness against the development of diseases such as type 1 diabetes, rheumatoid arthritis and lupus. These so-called autoimmune diseases occur when your immune system attacks your body’s own tissues, but the study results indicate that these diseases could be treated with medications that exist today, which force long-lived immune system cells to die.
When your immune system is developing, it produces some cells that have the potential to attack the body’s own tissues, which causes autoimmune diseases. However, when these ‘self-reactive’ immune cells die through a process called apoptosis, you are more protected against autoimmune disease. Yet this study, which was published online in the journal Proceedings of the National Academy of Sciences, has shown that when your immune cells lack two related proteins, called Bax and Bak, they begin the process of attacking many healthy tissues, causing severe autoimmune disease.
According to Dr Lorraine O’Reilly, who was part of the study alongside colleagues Dr Kylie Mason, Dr Daniel Gray, Professor Andreas Strasser and Professor David Huang from the Walter and Eliza Hall Institute, and Professor Paul Waring from the University of Melbourne, Bax and Bak are part of a large group of proteins that control cell death, and the team found that some immune cells that lacked these proteins were able to attack healthy tissues in many organs of the body.
‘Normally, these ‘self-reactive’ immune cells are deleted during development. In the absence of Bax and Bak, enough self-reactive cells survive development to persist in the body and cause autoimmune disease in organs such as the kidneys (glomerulonephritis), similar to what is seen in the most severe form of lupus,’ O’Reilly reported.
She added, ‘Our findings confirm that defective apoptosis of immune cells can cause autoimmune disease, and that Bax and Bak are important determinants of immune cell death. We were also interested to see that, in our model, loss of Bak on its own was sufficient to cause autoimmune disease, albeit to a lesser extent than losing both Bak and Bax. This supports a recent discovery that humans with mutations in the BAK gene are predisposed to certain autoimmune diseases.’
She concluded by saying, ‘Our findings suggest that BH3-mimetics might be an exciting new option for treatment for autoimmune conditions, by activating Bax and Bak and making the self-reactive immune cells which are causing the autoimmune disease to die.’
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