Lyme Disease and Auto-Immune Dysfunction
When you get sick your body automatically turns on your immune system to fight infection and restore health (hence the term “auto-immune”.) Normally, the immune system can distinguish between “self” and “not self” and attacks those tissues that it recognizes as “not self.” (This is usually the desired response, but not always. For instance the body will attack a transplanted organ, or “reject” the organ. To prevent rejection, there are drugs that reduce the activity of the immune system called immunosuppressants.)
With Lyme disease, there has been great debate whether Chronic Lyme Disease (CLD) is due to persistent bacterial infection, or to the body’s ongoing autoimmune activity, or rather hyper-activity, where the immune system continues to attack the tissue where the spirochetes resided – even after they are destroyed.
A passionate immunologist, Janet Weis, PhD, from the University of Utah has been studying this puzzle since 1992 using generations of mice who have been carefully bred and cataloged to represent a dizzying selection of every conceivable cross-section of immune system strength measured by inflammation.
So the mice prone to no inflammation represented marginal immune system response and those mice prone to severe inflammation represented hyperactive immune system response.
Her studies involve injecting the mice with Borrelia and recording the immune response from the moment of infection over months of disease. With over 400 mouse lines to compare the results were surprising and amazingly consistent.
First, she learned that the mice were damaged before the immune system response which effectively settled the original question.
Furthermore, she found that although it was true that a severe immune response was destructive, the lack of response was even more destructive, and produced the sickest mice. This reflects the widely diverse response in us.
Following these discoveries, Dr. Weis began to study the exact molecular process that initiated the inflammation in Lyme disease. Her discovery of “TLR2” (Toll Like Receptor 2) explains how the Borrelia proteins latch on to healthy cells to instigate the inflammation process.
What does all this mean to those of us with Lyme disease?
First, it proves the complexity of the disease which is at the heart of the overarching medical debate about treatment. Science can show why Lyme infection persists even after treatment corresponding to the published standard of care.
What I find even more exciting is the new avenue of study which will hopefully allow science to find a permanent cure.
Read more about Janet Weis and her research here.
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November 7th, 2008 at 10:02 pm
I suffer from neuro lyme