Molecular mimicry has been mentioned here on the board before, but we have never pursued it in much depth. I have a hunch that may well be the actual cause of the autoimmune reactions that cause our inflammation. This supports the theory that Polly and I, (and others), have long held, that some pathogen is responsible for triggering the autoimmune response that leads to microscopic colitis. The fact that many of us also experience symptoms of arthritis, and various other autoimmune diseases, as side effects of MC, lends support to the theory that molecular mimicry may be at the source of our problems.
Basically, molecular mimicry is defined as the theoretical possibility that sequence similarities between foreign, and self-peptides, ("self" refers to our own body), are sufficient to result in the cross-activation of autoreactive T or B cells, by peptides produced by, or found in or on, pathogens. IOW, molecular mimicry is/may be an occurrence in many autoimmune disorders, in which a microbe carries antigens that resemble those on a particular organ, causing the immune system to attack the body.
Rotavirus is a very common cause of gastroenteritis, (inflammation of the stomach and intestines). It's commonly referred to as the "stomach flu", though it has no relation to influenza. The theory is that some of us are more vulnerable to "complications" resulting from it than others, (possibly due to genetics), and repeated infections appear to make one more vulnerable to the development of autoimmune diseases, possibly through the mechanism of molecular mimicry.
Consider this quote from the article linked to below:
http://stanford.wellsphere.com/digestiv ... you/370758Two recent scientific publications have now shown that a rotavirus (common gut viral infection) protein may be linked to celiac disease through a “molecular mimicry” mechanism. “Molecular Mimicry” describes a phenomena whereby some pathogens like viruses, yeast or bacteria, can evoke an immune response because they have enough similarity to the body’s own proteins to cause an autoimmune reaction. This is evident in a number of autoimmune disorders associated with certain HLA genotypes (susceptibilty genes) such as in rheumatoid arthritis (RA) or Ankylosing Spondylitis (AS). In some cases of AS or RA, gut bacteria that passes through the gut barrier and is recognized by the immune system as “similar” to joint tissues. As the immune system reacts to the bacteria to eliminate it, it actually attacks the joint isssue. In the case of a rotavirus infection, a common cause of gastrointestinal infection and inflammation (gastroenteritis), it is seen as a similar to the gialdin molecule and the body is triggered into the same intolerance, or immune reaction as stimulated by gliadin in susceptible individuals. Antibodies to this celiac peptide also recognize and bind to the rotavirus protein (VP-7) and cause the same leaky gut/intestinal permeability that is a key step in the immune activation associated with CD.(19) Thus, viral infection and/or tissue damage in the intestine may cause inflammation and immune reactivity, leading to loss of tolerance for gluten. These recent studies on the link of a viral trigger in CD, provide the first indication that a high frequency of rotavirus infections may increase the risk of celiac disease autoimmunity in childhood in genetically predisposed individuals.(18) “Our findings show that in active celiac disease, a subset of anti-transglutaminase IgA antibodies recognize the viral protein VP-7, suggesting a possible involvement of rotavirus infection in the pathogenesis of the disease, through a mechanism of molecular mimicry.”(19)
We've discussed the yeast connection before, several years ago, as a possible source of molecular mimicry which results in the body's immune system perceiving wheat as a foreign threat, (candida yeast).
http://www.perskyfarms.com/phpBB2/viewt ... ar+mimicry
Here's a long research article that concludes that rotavirus infections may be causative of celiac disease. Researchers discovered that antibodies from blood provided by patients with celiac disease, (when they were eating food containing gluten, and when they were on a gluten-free diet), contained a "celiac peptide", (a synthetic protein fragment that was recognized only by the antibodies made by patients with active disease), and by searching a database of pathogen proteins, they discovered that rotavirus protein VP-7 contains a very similar peptide. Furthermore, a search of a database of human proteins showed that this celiac peptide also resembles peptides found in human tissue transglutaminase, (Toll-like receptor 4, and several other self-antigens). The researchers demonstrated that patient antibodies which bind to the celiac peptide, also bind to VP-7, and to these self-antigens, and only patients with active disease made these antibodies. They therefore concluded that:
http://www.plosmedicine.org/article/inf ... ed.0030358Our findings show that in active celiac disease, a subset of anti-transglutaminase IgA antibodies recognize the viral protein VP-7, suggesting a possible involvement of rotavirus infection in the pathogenesis of the disease, through a mechanism of molecular mimicry. Moreover, such antibodies recognize self-antigens and are functionally active, able to increase intestinal permeability and induce monocyte activation. We therefore provide evidence for the involvement of innate immunity in the pathogenesis of celiac disease through a previously unknown mechanism of engagement of Toll-like receptor 4.
So far, there's no real proof that molecular mimicry could result in the development of celiac disease, MC, Crohn's, UC, or any other autoimmune disease, but it looks very, very suspicious, doesn't it. One would hope that researchers would pursue this line of reasoning.
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