Autoimmune thyroid diseases, such as Hashimoto’s thyroid disease and Graves’ disease, are several of the most prevalent causes behind thyroid gland dysfunction. Autoimmune thyroid diseases, or AITDs, occur when the human body’s own immune system attacks and damages a healthy thyroid gland. It’s this autoimmune assault on the thyroid which can, over time, lead to the overactive or the underactive function of the buttefly-shaped gland in our neck.
According to numerous research studies, autoimmune thyroid diseases can be caused due to a variety of factors. Environmental factors like iodine intake and selenium deficiency can alter the balanced metabolism of chemicals in the human body necessary for the proper function of the thyroid gland. Additionally, environmental factors such as exposure to environmental pollutants and toxins have been linked to the interference of efficient thyroid hormone secretion.
One autoimmune thyroid disease trigger, however, is often overlooked by healthcare professionals; infection. Researchers today still do not fully understand how infections trigger autoimmune diseases, however because our immune systems are so complicated and every disease is unique, it’s very likely that there are a number of variables. Recent studies have identified three theories which explain the links between infections and AITDs.
Autoimmune thyroid diseases triggered by molecular mimicry are virtually hypothesized to occur when the infection is structurally similar to that of the thyroid gland. Therefore, once the network of defense cells, tissues and organs activates, the immune system proceeds to strike the infection and attacks your thyroid gland.
In this circumstance, the immune system activates when a virus or bacteria invades the thyroid gland and sends cells into your thyroid to destroy the infection. While these cells are currently all attacking the bacteria or virus, it injures the thyroid gland. More cells are signaled by the inflammation to the thyroid gland where they often continue to attack.
You can think about this as the “hijacking theory” where an infection (usually due to a virus) hijacks the thyroid cells’ DNA to hide from your immune system. The immune system is intelligent enough to detect the virus anyway, and strikes the virus as well as the thyroid cells it is hiding in.
In certain individuals, autoimmunity is the price to be paid for the eradication of an infectious agent. Infections are implicated in the pathogenesis of endocrine, and nonendocrine diseases. Either fungal or viral diseases may represent a risk factor for the evolution of AITDs. Viruses have long been suspected as etiological agents in a variety of health disorders, uncluding autoimmune thyroid disease; furthermore, a trigger of AITDs, infecting the thyroid or immune cells, was demonstrated in an avian model. This potential remains unproven although viruses may be agents in AITDs.
An increased frequency of antibodies to the influenza B virus has been observed in a group of patients with thyrotoxicosis. Virus-like particles have been discovered in the thyroid of chickens together with similar particles. Serological evidence of staphylococcal and streptococcal disorders were described in a few patients with AITDs.
Some of the strongest evidence linking infectious agents to AITDs’ induction has been the institution of Yersinia enterocolitica disease with thyroid disorder. This Gram-negative coccobacillus commonly causes diarrhea along with a number of abnormalities that indicate disorder, including arthritis, arthralgias, erythema nodosum, carditis, glomerulonephritis, and iritis. Weiss et al. demonstrated that Y. enterocolitica needed a saturable, hormone-specific binding site for its mammalian TSH that resembled the receptor for TSH from the human thyroid gland.
An immune response against a viral antigen that shares homology with the TSHR might be the inductive event that ultimately leads to autoimmunity. A substantial association between AITDs and hepatitis C has also been found. Antibody titers are shown to increase in patients with the hepatitis C virus, and these patients were more susceptible to AITDs than were hepatitis B sufferers. These patients must be screened for autoimmune thyroid disease.
Infection might induce an autoimmune response by various mechanisms, such as polyclonal T cell activation by microbial superantigens mimicry, and thyroid expression of human leukocyte antigens. Inflammation can alter cell signaling pathways and influence T cell activity and cytokine secretion profiles.
In conclusion, research studies have shown that autoimmune thyroid diseases may also be the response of environmental factors such as infections. Infections can lead to AITDs when the human body’s own immune system attacks and damages the thyroid gland cells in addition to those of bacteria and viruses. Ultimately, treating bacterial and viral infections can be an essential way to prevent autoimmune thyroid disease or complications.
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By Dr. Alex Jimenez
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