(dailyRx News) We think of the immune system as our body's white knight - our protector from invaders. It turns out that this knight has a deadly side as well. Early research indicates a way of harnessing both powers could lead to new healing therapies.
A molecule has been found that helps to either rev up the immune system or clamp it down.
This discovery could lead to the development of drugs that may be useful in fighting cancer and preventing organ transplant rejection.
Loyola researchers, led by Makio Iwashima, PhD, an associate professor in the Department of Microbiology & Immunology, have found that manipulating a molecule known as transforming growth factor beta (TGF-β) could open important new therapeutic doors.
The immune system has two types of cells:
- Effector cells are the body's white knights, attacking both tumor cells and infected cells.
- When effector cells are overactive, a person can have autoimmune disease such as multiple sclerosis or lupus.
- Regulatory cells control and dampen the immune system so it doesn't attack healthy tissue.
- When regulatory cells are too active, the immune system is too weak to fight off against germs and cancer.
Now the TGF-β is a regulator cell which normally controls or suppresses the immune system response.
For this study, researchers found this molecule can ramp up the immune response to become more targeted and effective in certain conditions. The TGF-β can also dial down the immune system.
Iwashima explained, "TGF-β is a double-edged sword. It augments immune system reactions but does not determine what direction they will take. Depending on conditions, these reactions can either activate or suppress the immune system."
This was demonstrated in mouse cells treated in petri dishes. Further study will involve examining TGF-β in human cells and later in animal studies.
This knowledge may then be used to develop drug therapies that either activate or tamp down the immune system, as needed, according to Iwashima.
This research was published online April 13, 2012 ahead of print in the Journal of Immunology
The study was supported by the National Institutes of Health and the Van Kampen Cardiovascular Research Fund.