Molecular mimicry is when one molecule mimics another one in the way it behaves in the body. Specifically, it’s when the immune system mistakes one antigen (or potential pathogen) for another.
But before I explain how this can lead to autoimmunity, allow me to recap how the immune system works.
When you first get infected with a bacteria or a virus, prowling cells called macrophages will notice that it looks fishy, and will gobble it up. Then they’ll post segments (or antigens, usually about 10 amino acids long) of what it just ate on its surface, so that the circulating T-cells (part of your body’s specific immune system) can have a good look at it. A T-cell with a receptor that matches the presented antigen will lock onto it, and will then in turn tell the B-cells to make lots of antibodies against that antigen—or (and here’s the important part) against any other protein with an amino acid sequence or confirmation that behaves like that antigen.
The B cells make antibodies against three different types of antigens:
- Soluble antigens: these come from food.
- Insoluble antigens: these come from infectious agents like viruses and bacteria.
- Self antigens: these are to your own tissue.
How Molecular Mimicry Triggers Autoimmunity
The idea that molecular mimicry could play a role in autoimmunity was first proposed back in 1985. It was once thought highly improbable from a statistical standpoint, just because the probabilities of two antigens having exactly the same 10 amino acid sequence was so low.
However, it’s now understood that mimicry doesn’t have to mean two proteins share exactly that sequence; sometimes the structure of two antigens (the way they each fold in three-dimensional space) might be similar enough that the antibody might fit them both, thus triggering an immune attack.
Another possibility is that the two antigens, though dissimilar in sequence, might have a similar charge signature (i.e. they’re positive and negative in the same places) or a similarity in polarity (i.e. the way the antigen interacts with water), and these might be enough to trigger mimicry, such that the antibody designed for a pathogen might fit either a food antigen or a self antigen as well.
Well-known examples of this process include:
- Celiac Disease. Three-way mimicry may occur in Celiac, in which part of the gliadin molecule (found in gluten) looks very much like part of the lining of the small intestine, and also very much like a segment of adenovirus 12 and Hepatitis C.
- Rheumatoid Arthritis. More than one virus is implicated in mimicry setting off RA. Bacterial imbalance in the gut may also be a contributing factor, perhaps explaining the link between allergenic foods and worsening RA symptoms.
- Type 1 Diabetes. Group B coxackievirus, rotavirus, and influenza A viruses are all implicated in the pathogenesis of Type 1 Diabetes; apparently antigens from each of these viruses and more look similar enough to the beta cells of the pancreas to trigger autoimmunity in susceptible people.
- Myasthenia Gravis. More than one virus may trigger Myasthenia Gravis, an autoimmune condition that generates antibodies against the receptor for the neurotransmitter acetylcholine, controlling muscles (among other things).
- Multiple Sclerosis. Apparently Epstein Barr is associated with MS, with antigens similar enough to the myelin coverings for our nerves sufficient to set off the process in susceptible individuals. This interesting article suggests the heat shock proteins generated from a number of infectious agents may be responsible, though.
Why Do Infections Trigger Autoimmunity in Some People and Not Others?
Genetics definitely play a role in this process: specifically, they help to determine which amino acid sequences the macrophages present to the T cells, thereby triggering which T cell fits and the exact appearance of the antibodies against a particular pathogen that an individual produces. (Remember the analogy of three blind man feeling an elephant and trying to determine what it looks like based on whether they’re touching its trunk, its hide, or its tail? Same concept.) This is why some people who have been infected by adenovirus can still eat gluten and be just fine, while others develop Celiac Disease (though I think there are other reasons for the 400% explosion in Celiac since the end of WWII, too—read here for more on this.)
What to Do With This Information
I wrote this article as an addendum to this one on the Autoimmune Protocol, in order to further explain what I said about avoiding not just gluten, but gluten cross-reactive proteins (those foods that look like gluten to the immune system, such as oats, millet, soy, corn, rice, yeast, and potatoes) if you’re susceptible to gluten… or if you have an autoimmune disease and don’t know if you are specifically triggered by gluten or not. This is an especially good idea for Celiac patients who are avoiding gluten and still struggling.
This is also useful information in treating other autoimmune conditions as well, if the pathogen triggering autoimmunity is still present (in the gut flora for instance, as this article suggests). I always run a comprehensive stool culture to find out what kind of bacterial pathogens are hanging out in the gut for people who have any kind of autoimmunity, in addition to checking for foods to which the body produces antibodies. All of these may perpetuate the production of self-antigens, and addressing them can be very effective in helping to restore health.