What is the relationship between the thyroid and the immune system?
The thyroid and the immune system are closely intertwined: dysregulated T immune cells cause the most common thyroid diseases, and selenium supplementation can measurably dampen the immune response in Hashimoto's disease, although medical supervision is advisable.
In autoimmune thyroid diseases, the body's own immune system attacks the thyroid gland. The two best-known forms are Hashimoto's disease, in which the thyroid is gradually destroyed and becomes underactive, and Graves' disease, in which the thyroid becomes overactive instead. Both diseases are driven by T immune cells that infiltrate thyroid tissue.
How that attack process works has been well mapped out. Certain T immune cells (Th1 and Th17) produce pro-inflammatory substances that amplify the inflammation in the thyroid and further reinforce themselves. At the same time, regulatory T cells decrease -- the brake on the immune system. That disrupted balance drives the disease further. Genetic predisposition plays a clear role, but there are also environmental factors that increase the risk: a deficiency of vitamin D, selenium, zinc or magnesium, infections, chronic stress, smoking and a disrupted gut microbiome.
Of all those environmental factors, selenium is the best studied as a means of intervention. In a randomised trial involving 90 patients with Hashimoto's disease, six months of selenium supplementation led to a measurable reduction in thyroid antibody levels, and the proportion of regulatory T cells increased. Patients in an early stage of the disease appeared to benefit the most. For the other deficiencies (zinc, magnesium, vitamin D), an association with disease activity is visible, but whether supplementation actually helps has not yet been convincingly demonstrated for most of them.
People with an autoimmune thyroid disease also have an elevated risk of other autoimmune conditions, such as rheumatoid arthritis, lupus or Sjogren's syndrome. An observed association with papillary thyroid cancer has also been noted. This means that regular monitoring for thyroid nodules and other autoimmune complaints is worthwhile.
The relationship between the gut microbiome and thyroid autoimmunity is being investigated. A disrupted gut microbiome appears to adversely affect the T cell balance, and thyroid hormones in turn influence the gut microbiome. Cause and effect have not yet been disentangled in humans, so concrete advice about probiotics or diet for the thyroid remains premature.
Five PMIDs with moderate to strong evidence on autoimmune thyroid diseases; one small RCT on selenium (n=90); one early observational study on the gut microbiome; one early tissue biopsy study on thyroid cancer and immune evasion.