Scientists in Canada think they may be on the verge of being able to “supress” over-reactive cells in the body that lead to autoimmune disorders such as Alopecia Areata, which causes sudden, patchy hair loss.
According to a new report from the team at the Research Institute of the McGill University Health Centre in Montreal, regulatory T Cells also known as Tregs ("tee-regs") play a key role in managing the body’s response to potential threats. When Tregs are not functioning properly, the body can “over-react” and start attacking when there is no need. This is the essence of an autoimmune disorder.
is the second most common cause of hair loss after androgenetic alopecia - more commonly known as male and female pattern baldness. It is estimated to affect around three per cent of people at some point during their lifetime, worldwide.
It has a number of suspected triggers, including physical trauma (such as a car accident), shock and sudden extreme stress (such as a bereavement) and long-term psychological stres, though the underlying biological mechanism that causes this form of autoimmune hair loss remains unknown. Accordingly, people who visit a specialist clinic for Alopecia Areata treatment can be frustrated as to why they are not given a precise reason as to what caused their hair loss, only what is likely to have triggered the issue.
Like all autoimmune disorders, alopecia areata is complex, and research aiming to establish more about the enigmatic condition is underway in a number of countries. Additionally, as there are currently only effective alopecia areata treatment solutions for the patchy, scalp-only variant, the medical community is highly focused on helping those with the presently untreatable, more extreme versions Alopecia Totalis and Alopecia Universalis. These cause sudden hair fall from the whole head, and from head to toe respectively. By understanding more about how autoimmune hair loss works, it is more likely that effective treatments for all severities will be discovered. For this reason, research like that of the Canadian team is vital.
The researchers were investigating a rare mutation in a gene called FOXP3 which they found to affect the Treg cell’s ability to dampen the immune response. This, said the study’s lead author Dr Ciriaco Piccirillo, “results in the immune system overreacting and causing inflammation. This discovery gives us key insights on how Treg cells are born and how they can be regulated.”
His colleague, Khalid Bin Dhuban, added that: “Understanding this specific mutation has allowed us to shed light on how many milder forms of chronic inflammatory diseases or autoimmune diseases could be linked to alterations in FOXP3 functions.”
Inspired by its findings, the team went on to develop a molecule that could restore the Treg cells’ ability to control the immune system for patients with the same mutation. It has now been tested in animal models, and the researchers now hope to develop new drugs that will work with other conditions where defective Treg cells are thought to be an issue.
What’s important, of course, is that new drugs don’t take things too far and inadvertently turn off the whole immune system. As Dr Piccirillo says: “Our goal is to increase the activity of these Treg cells in certain settings, such as autoimmune diseases, but we want to turn it down in other settings, such as cancer.”
While Alopecia Areata is just such an autoimmune disorder that might benefit from the team’s work, there appears a chance that developments in Treg research may even throw some light on possible new treatment options for genetic shedding conditions such as Male Pattern Hair Loss. A recent study by the University of California, San Francisco, found that defective Tregs may also play a part in genetic thinning, too.
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