Why does autoimmune thyroiditis develop?

The autoimmune process develops when there are antibodies to the cells of one's own body. In the presence of antibodies to thyroid cells, autoimmune thyroiditis develops. The disease is also called lymphocytic thyroiditis or Hashimoto's goiter. Autoimmune thyroiditis is characterized by the gradual destruction of thyrocytes with the development of a hypothyroid state. This disease is detected in 10% of the total population, more often in women. What mechanisms and reactions lead to the development of autoimmune thyroiditis?

What are the causes of autoimmune thyroiditis?

Hashimoto's goiter refers to genetically determined diseases. Pathology can be traced in blood relatives and often manifests along with other autoimmune diseases. The implementation of genetic propensity occurs under the influence of various environmental factors. How environmental factors affect the development of pathology, estet-portal.com knows. They induce autoaggression, which provokes the gradual and complete destruction of thyrocytes. With age, the number of autoantibodies increases, which is associated with the summation of negative factors and impaired immune regulation.

Among all chemical elements, iodine leads to the induction of autoimmune thyroiditis. At the same time, the physiological norm of iodine does not provoke the development of an autoimmune process. It develops in the presence of an amount of iodine that is thousands of times higher than the allowable norm.

An increase in the number of patients with autoimmune thyroiditis testifies to the effect of biological factors  after seasonal exacerbations of respiratory diseases.

Description of the mechanism of development of autoimmune thyroiditis

Normally, a small amount of auto-aggressive lymphocytes is formed in the bone marrow. They are inactivated as they pass through the thymus. Thus, the central mechanisms of immunological tolerance are realized. If some antigens are absent in the thymus, then lymphocytes leave it and react with antigens in the periphery, becoming anergic. This is how the peripheral mechanisms of immunological tolerance are realized.

It is these mechanisms that are violated in autoimmune thyroiditis. Partial deficit T – suppressor allows the survival of "forbidden clones" T – lymphocytes. They interact with thyrocytes, provoking a delayed-type immune response. T-helpers interact with B – lymphocytes and promote their transformation into plasma cells, which is accompanied by the production of antibodies to thyroglobulin and thyroperoxidase.

The role of circulating antibodies in the development of autoimmune thyroiditis:

• interact on the surface of thyrocytes with T – killers;
• have a cytotoxic effect;
• cause destruction of thyrocytes.

Pathogeny of the development of atrophic and hypertrophic forms of autoimmune thyroiditis

Over time, the synthesis of thyroid hormones gradually decreases, the release of thyrotropin is activated by the feedback mechanism. This leads to an increase in the size of the gland and the development of a goiter.

This is how the hypertrophic form of autoimmune thyroiditis develops. Thyroid tissue has a high regenerative capacity, thanks to which this process lasts for decades.

Besides regeneration, thyrocytes express some proteins on their surface that turn autoaggressive lymphocytes into anergic ones. The duration of the thyroiditis process depends on the predominance of destruction or regeneration processes. In the presence of blocking antibodies to thyrotropin, an atrophic form of autoimmune thyroiditis develops. The studies revealed a high titer of antibodies to thyroglobulin. Thus, the processes of development of autoimmune thyroiditis occur.

Read about the clinical manifestations, diagnosis and treatment of autoimmune thyroiditis in our next article.