Cross-Reactivity and the Immune System
The effects of gluten on the immune system and can confuse the inflammatory cells into harming our body. Our body’s immune system evolved towards preventing any foreign substance, bacteria or virus from repeatedly initiating the same reaction or consequence in our bodies. For example, we are susceptible to the chicken pox virus only once in our entire life. If it re-emerges later in life, it is due to our immune system weakening as we age or if we are immune-compromised.
Basically, our body’s inflammatory cells will identify the virus and assign certain cells to evolve to specifically beat the virus. These cells will remain in our body and will always be prepared for another invasion of chicken pox. When it happens, the body will react right away and leave us with nothing more than a slight cold or fever at worst.
Paradoxically, this same efficiency of our body’s immune system can also be detrimental to our health. The chemicals that the inflammatory cells release in order to defeat offending substances or organisms can also damage neighboring cells or tissues. Aside from this, our inflammatory cells can be hyper-responsive to these offending substances. In effect, we have an excessively effective immune system.
Cross-reactivity occurs when two substances with near-identical protein structures incite a similar reaction from the body. Gluten, for example, is a type of food protein that triggers a violent reaction. Naturally, the body will try to prevent such a reaction from occurring. When a substance with a similar protein configuration comes in contact with the cells of the gut, the inflammatory cells will react as if they had been overwhelmed with gluten.
A classic example of a protein that causes cross-reactivity is casein. This is a protein which can be found in most dairy products. Patient’s presenting with gluten-sensitivity often evince a similar sensitivity to casein as well because of their similarity in protein structures. Gluten and casein have similar molecular components and structure. They also have similar by-products after they have been metabolized – gluteomorphin and casiomorphins. These morphins produce decreased alertness, faulty memory and diminished concentration.1
Another main reason this occurs is the destruction of the intestinal villi which gluten causes in the intestinal walls. When this happens, the body is unable to produce the enzyme lactase which helps our body digest dairy products. Because of the decrease in lactase production, the body is unable to digest lactose which leads to lactose intolerance. Even after switching to a gluten-free diet, the body takes roughly a year to repair the damaged intestinal cells and produce an adequate amount of lactase once more. Thus, for patients who present with lactose intolerance combined with gluten sensitivity, a gluten-free and casein-free diet is prescribed.2
Molecular Mimicry and Autoimmune Diseases
Molecular mimicry rests on the observation that a similarity between two peptides can lead to a cross-activation of T-cells and B-cells which are “autoreactive”. This concept involves two peptides, one foreign and the other self-generated and presumably safe. This means that a foreign substance can activate the T-cell or B-cell to attack not only itself but a peptide that is naturally occurring within our body.3
Activation of these cells need not come from peptides which have the exact same sequence as the self-generated peptides. As long as a few crucial amino acid residues are similar between the two peptides, it is sufficient to activate either a single antibody or a T-cell receptor (TCR). When these T-cells or B-cells are activated, it is proposed that they are “tricked” into believing that self epitopes (peptides which are similar to those offending agents) are its target and this causes what we know as autoimmune diseases and the resultant tissue pathology.4
Molecular mimicry is one of the proposed phenomena in which autoimmunity occurs. Instead of limiting the damage to the foreign or offending substance, the inflammatory cells are tricked into attacking our own cells. The process is due to the failure to recognize self antigens or peptides as endogenous. This leads to loss of immunological intolerance, which is the capability of discriminating self from non-self.5
Cross-reactivity and Molecular mimicry are nearly the same. The difference is their targets. In cross-reactivity, the inflammatory cell targets a food product which is similar to the nutrient you are allergic to. An example is the aforementioned similarity in response to both gluten and casein. Molecular mimicry, on the other hand, targets our body’s own cells such as the renal, intestinal or joint tissues of our body. When this occurs, diseases such as Hashimoto’s and rheumatoid arthritis could occur. When the thyroid tissue of patients with Hashimoto’s disease are examined, there is an over-abundance of inflammatory cells which causes the patient to be hypothyroid. This means the immune system attacked the patient’s own thyroid tissue thinking it is a foreign or dangerous organism. When this occurs, this causes an imbalance in the patient’s metabolism. This causes the patient to become lethargic, fat, and slow.
The same thing happens in gluten sensitivity. Patients who eat gluten, corn, milk or any similar substance can trigger not only to cross-reactivity but also molecular mimicry. This is one of the main issues of celiac disease. Because it is an autoimmune disease, it causes the body to cross-react to similar substances and also lead to the destruction of self-tissues. This includes the body’s joints and intestinal tissues which leads to the obvious symptoms of the disease.
- Osborne, P. (2013). How cross-reactivity, molecular mimicry, and mold toxicity can seriously impact your health. ↩
- Pettersen, V. (2009). Gluten and casein intolerance. Retrieved from http://www.glutenfreefox.com/articles/gluten-and-casein.html ↩
- Kohm, A.P., Fuller, K.G. and Miller, S.D. (2003). Mimicking the way to autoimmunity: an evolving theory of sequence and structural homology. TRENDS in Microbiology 11 (3): 101–105. ↩
- Abbas, A.K. and Lichtman, A.H. (2005). Cellular and Molecular Immunology: Updated edition. Elsevier. Philadelphia, PA. pp. 216–217. ↩
- Shoenfeld, Y. and Gershwin, M.E. (2002). Autoimmunity at a glance . Autoimmune Reviews 1: 1. ↩