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The process of molecular mimicry is deceivingly simple but entails a lot of understanding of the workings of the immune system. Basically molecular mimicry means that part of a molecule of a given protein closely resembles a part of another totally different protein. Proteins are made up of strings of amino acids and in molecular mimicry one series amino acids(eg~10) in one protein is very similar to a string of ten amino acids in another protein. Given that there are 20 different amino acids it is a rather rare occurrence to find such mimicking arrangements but many examples have been demonstrated.

The main types of proteins which came into play in autoimmune disease are:
1. self proteins which are part of the human body. An example of this would be myelin basic protein which is the most common protein in myelin and the GAD protein of the pancreas;
2. proteins of infectious agents such as viruses and bacteria;
3. food proteins. For example over 400 different proteins occur in cow's milk and most have over 150 amino acids.

To understand how molecular mimicry works in the induction of autoimmunity one must understand the basic mechanisms of an immune response to a foreign invader in the body. The immune system recognizes a part of the protein portion of the invader. It does this with T cells which have receptors which bind to short segments(~10 amino acids) of a foreign protein. A macrophage will engulf a foreign invader (e.g. a bacteria or food particle) and break it down into fragments.

A special molecule in the macrophage then carries a protein fragment(peptide) to the surface of the cell and "presents" it to the millions of circulating T cells. A T cell which has a matching receptor locks onto the presented protein fragment. The T cell then becomes activated and stimulates other portions of the immune system to begin an immune response against all proteins which contain a similar looking amino acid string. The details of what constitutes a similar looking string are beyond this summary but suffice to say it has been found that a variety of similar, yet somewhat different strings, can be recognized by the same T cell.

Thus, it is easy to understand how molecular mimicry can trigger an autoimmune reaction. If the protein fragment from a foreign invader which is presented to the T cell closely resembles part of a self protein then the activated immune system will not only attack all foreign invaders which have the same string of amino acids but will also attack a very similar string in a self protein. It has been shown that parts of proteins in various foods and infectious agents resemble parts of various self proteins. Sometimes a three way mimicry occurs with a protein fragment from a food closely resembling that of an infectious agent which in turn closely resembles part of a self protein.

In Children with Autoimmune Disease, Response Starts Early

Newswise - Children with neurological autoimmune diseases develop immune reactions to other targets in their bodies and in food early in their disease, according to research that will be presented at the American Academy of Neurology 58th Annual Meeting in San Diego, Calif., April 1 - 8, 2006.

T cells are the body's regulators of the immune response. Increased T cell proliferation is a characteristic of autoimmune disease, in which the immune system attacks body tissues.
However, it wasn't known whether this increased proliferation occurred early, or as a result of chronic autoimmunity, said lead researcher Brenda Banwell, MD, from the Department of Pediatric Neurology at the Hospital for Sick Children in Ontario, Canada.

The researchers studied 166 children: 63 with an autoimmune demyelinating syndrome (either multiple sclerosis or an isolated event of central nervous system autoimmunity), 43 with type I diabetes (also an autoimmune disease), 31 with a non-autoimmune neurological condition, and 30 healthy controls. They examined blood samples for T cell proliferation in response to exposure to a variety of antigens (targets), including myelin protein from nerve cells, proteins in the pancreas, and proteins in milk.

As expected, more children with central nervous system autoimmunity had T cell proliferation after exposure to myelin than control children (50 percent versus 10 percent). About a quarter of these children also showed a response to proinsulin, a T-cell target in type I diabetes. Over sixty percent also responded to a protein in milk. Ninety percent of the children with type I diabetes responded to pancreatic antigens as expected, but almost as many (79 percent) responded to myelin, and 90 percent responded to milk protein.

Even at the onset of their disease, children with autoimmune diseases harbor T cells that will react against proteins within their tissues, Banwell said. The responses seen against milk proteins raise the possibility that substances in food may be associated with autoimmunity.