No one really knows what causes the immune system to mount an attack on platelets or other needed body part. Here are some general theories on the causes of autoimmune diseases. Although these are presented as three theories, they can be viewed as pieces of a larger puzzle.
Molecular Mimicry Theory
This theory suggests some autoimmune diseases may be caused when a person’s immune response gets confused between its own cells and invading virus and bacteria if the invaders are similar to the host cells.
When a virus invades our body, special cells chop it up into thousands of fragments and put some of them in a type of pocket for the immune system to disable. A person’s genes determine which of the invader fragments go in the pocket. T-cells latch on to the fragments in the pocket and send signals to destroy all of the tissues that have that type of fragment.
The problem comes when some part of the body has the same amino acid sequence on its surface as the invader fragment. When this happens T-cells attack the ‘good’ cells with the twin fragments as well as those with the pocketed viral fragment. Another study suggests that the good cells might not need the same amino acids sequence, perhaps just having another similar property, such as a negative charge, can create the same confusion. This means that a larger number of proteins with different amino acid sequences can stimulate the same T-cell, setting off an autoimmune disease.
According to the research scientists, the disease process involves many more steps. The bad luck may unfold over several years and require multiple infections and a genetic predisposition to activate.
"Virus’s Similarity to Body’s Proteins May Explain Autoimmune Diseases"12/31/96, New York Times
Richard Aster; “Molecular mimicry and immune thrombocytopenia,” Blood, 23 April 2009, v. 113, no. 17, p. 3887
Wei Zhang, et al; “Role of molecular mimicry of Hepatitis C virus protein with platelet GPIIIa in Hepatitis C-related immunologic thrombocytopenia” Blood 23 April 2009, Vol. 113, no. 17, pp. 4086-4093. http://www.ncbi.nlm.nih.gov/pubmed/19023115
Free Radical Damage
In this theory, the DNA in our cells can be altered or destroyed by reactive substances in our bodies. When the destroyed DNA is a part of the immune control function, it can result in a specific autoimmune disease.
Free radicals are particles with an unstable molecular structure that act as scavengers in the body and rob electrons from other molecules to increase their stability. The particles that are robbed don’t function as they should and can be toxic. Free radicals build over time since they are a natural byproduct of our metabolism and a general component of aging. Their production is hastened by stress, pollution, fertilizers, pesticides, prescription drugs, alcohol, electromagnetic radiation, etc.
Our bodies have built-in controls for free radicals and ways of changing them into neutral substances. These detoxification mechanisms require specific enzymes to make them function well. If our bodies do not have the vitamins and minerals to make up the enzymes, or if the detoxification mechanism is damaged, perhaps by free radicals, the result is a surplus of free radicals and other toxic substances. This can also happen if our lifestyle and environment create more toxins than even a good working system can neutralize.
The excess free radicals and other noxious byproducts of a failed detox process roam our bodies and attack our weakest links. These weak links may be due to genetics. They may be other parts of our immune system that happen to be nearby. Depending on the DNA attacked, the electron grabbing can cause an autoimmune disease.
(Summarized from Sharma, Hari, M.D. Freedom from Disease, Toronto, Ontario:Veda Publishing, 1993, Rogers, Sherry A, M.D., Tired or Toxic? A Blueprint for Health. Syracuse, NY: Prestige Publishing, 1990, and a conversation with a research scientist at Rutgers University)
Microbial Trigger Theory
Scientists have discovered that we have immune cells which, when activated, can target the body’s own molecules. Researchers at the National Institute of Allergy and Infectious Diseases, Yale University, and Duke Medical Center, among others, have found these cells can be activated by bacteria, at least in mice.
When it is fighting a reaction, the body produces a compound called interleukin-12 during its normal immune response. Interleukin-12 then creates many other immune compounds specific to a particular microbe. Researchers think this flurry of activity may activate any dormant self-reactive cells that may be near the infection. (If the self-reactive cell is for platelets, you get ITP)
(Summarized from "Microbial Trigger for Autoimmunity?" Science News, 6/21/97)
