Table of Contents
Introduction:
Autoimmune diseases are those in which the immune system damages the body's healthy cells. These diseases include rheumatoid arthritis, Crohn’s disease, and thyroid conditions. The immune system protects the body from diseases and infections. Hashimoto’s thyroiditis is an autoimmune disorder in which the immune system damages the thyroid gland.
What Is an Autoimmune Disease?
The immune system helps defend against diseases and infections. It identifies pathogens that enter the body and creates particular cells to fight against foreign cells. In the case of autoimmune disease, the immune system considers body parts such as skin or joints foreign. As a response, the immune system releases proteins called autoantibodies. These autoantibodies are responsible for attacking healthy tissue or cells. A few autoimmune diseases affect only one organ, whereas others may affect the whole body.
Causes of Autoimmune Diseases:
The exact cause of autoimmune disease is not known.
The factors involved in autoimmune disease include:
Gender: Females aged 15-44 years are affected more than males.
Family History: Genes that are inherited are responsible for autoimmune diseases. Environmental factors may also contribute.
Environmental Factors: Excessive exposure to sunlight, chemicals used for agriculture, mercury, cigarette smoke, and bacterial and viral infections like COVID-19 may increase the risk of autoimmune disease.
Ethnicity: Autoimmune diseases are more common in certain groups. White people from Europe and the United States (U.S.) are more susceptible to autoimmune disease. Lupus is more common among people of African, American, Hispanic, or Latino origin.
Nutrition: Nutrition plays a role in autoimmune diseases.
Other Health Conditions: Conditions like obesity may pose a risk for developing autoimmune diseases.
Symptoms of Autoimmune Diseases:
Different autoimmune diseases may exhibit common symptoms.
These include:
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Weakness.
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Experience dizziness and lightheadedness.
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Fever of low-grade temperature.
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Muscle pain.
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Difficulty concentrating.
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Experience numbness or tingling in hands and feet.
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Hair loss may be seen.
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Skin rashes appear.
Symptoms of autoimmune diseases may come and go, but in certain periods, they may flare up or appear to have increased. When symptoms appear, that period is called a flare-up; when symptoms are not present, such a period is called remission. The treatment depends on the disease. Treatment aims to slow down the immune system, which reduces the symptoms. Some people may require treatment for the rest of their lives.
What Is the Connection Between Hashimoto’s Thyroiditis and Autoimmunity?
Hashimoto’s thyroiditis (HT) is classified under autoimmune thyroid disease (AITD), which affects specific organs. It is estimated to affect 2-5 % of the population and includes HT and Grave’s disease (GD), among other conditions. HT is an autoimmune disease that causes the body's immune cells to kill cells that produce thyroid hormones. This decreases thyroid hormones, leading to hypothyroidism.
This disease reflects the loss of immunological response and shares the presence of a cell and humoral immune response against antigens from the thyroid gland with reactive infiltration of T cells and B cells and autoantibody generation. This further leads to the development of symptoms.
Lymphocytic infiltration is found to cause tissue damage and alter the function of the thyroid gland. The damage occurs when the autoantibodies and /or sensitized T cells react with the thyroid cells, resulting in an inflammatory reaction, and cell lysis may be observed in some cases. T-cell infiltration is mainly seen in HT.
Autoantibodies:
The thyroperoxidase antibodies (TPOAb) and TgAb (Tg antibodies) are considered the most common autoantibodies of the thyroid gland. TPOAb and TgAb are observed in individuals affected by AITD. These are found to be associated with complement-mediated cytotoxicity against thyrocytes. These are considered in the diagnosis of AITD. The absence of TPOAb and TgAb excludes the diagnosis of AITD. Their presence in the absence of the condition indicates a risk of developing an AITD.
TPOAb and TgAb antibodies are associated with thyroid dysfunction due to the use of some medications that can alter thyrocyte function. Increasing age is also a reason for the antibodies found in inherited individuals.
When the thyroid gland is completely removed, these antibodies disappear. This indicates that autoantigens trigger the antibodies. HT is chronic autoimmune thyroiditis or chronic lymphocytic thyroiditis. It is considered an organ-specific autoimmune disease that causes hypothyroidism in iodine-sufficient areas of the world. The surgeon Hakaru Hashimoto first described it.
It is estimated that HT affects 1 in 1000 individuals and affects 40 % of the elderly population of women. It affects women more than men, with a ratio of 18:1. Its peak frequency is forty years and above.
Pathogenesis:
A gradual loss of thyroid function, goiter, or both conditions can be noted as HT. The reason is autoimmune destruction of the thyroid gland. This is characterized by apoptosis of the thyrocytes.
Many mechanisms are involved in explaining the pathogenesis of HT. The first one is molecular mimicry. In this sense, HT is thought to be caused by an immune reaction against those antigens that mimic endogenous proteins in structure.
The second one is a virus entering the thyroid gland or activating non-specific lymphocytes within the thyroid gland, which may cause the release of cytokines. This triggers the thyroid-specific T cells and causes inflammation (thyroiditis).
The third one is the thyroid cell expression of HLA antigens. Genetics plays a role in the pathogenesis of AITD. HLA alleles are linked with AITD. It was noted that HLA DR3 and HLA DR5 are associated with HT. Individuals with HT express HLA II in thyroid follicular cells. INF-γ and other products from activated T cells or viruses induce these molecules called HLAII. Thyroid cells with HLA II become non-professional antigen-presenting cells.
The fourth one is thyroid cell apoptosis. In autoimmune thyroiditis, the cytokines are produced from antigen-presenting cells (APC) and Th1 cells. These cytokines can induce the expression of Fas and Fas ligands on thyrocytes and cause self-apoptosis.
Conclusion:
HT is a chronic autoimmune disease with no cure. The attack of healthy tissue causes an autoimmune disorder. In HT, the immune system attacks the thyroid cells that produce thyroid hormones, leading to hypothyroidism. This further affects many bodily functions. Hence, knowing about autoimmune disease and its connection with HT becomes important. Knowing about it may help identify the disease early. Early diagnosis leads to effective treatment, which further helps achieve a good quality of life.
