Hashimoto's and Graves' diseases both impair normal functioning of the thyroid gland but do so using different immunopathological mechanisms. Compare and contrast these mechanisms

Question

What will be an ideal response?

Answer 1

Both Hashimoto's and Graves' diseases disrupt the normal production of the thyroid hormones tri-iodothyronine (T3) and thyroxine (T4), which are derived from thyroglobulin in thyroid follicles. The formation of T3 and T4 requires engagement of the thyroid-stimulating hormone receptor (TSHR) with thyroid-stimulating hormone (TSH) secreted from the pituitary gland, a key step in the regulation of thyroid hormone production. This step malfunctions for these two diseases.
In Hashimoto's disease, anti-thyroid antigen antibodies and TH1 effector cells are involved. Large numbers of lymphocytes take up residence in the gland tissue, establishing germinal centers that resemble those in lymph nodes. Eventually the thyroid tissue is destroyed and thyroid follicles are no longer able to respond to TSH and make T3 or T4, a condition called hypothyroidism.
Graves' disease, in contrast, results in hyperthyroidism. Anti-TSHR antibodies act agonistically, mimicking TSH even in its absence. The thyroid follicle is chronically overstimulated by these antibodies and overproduces T3 and T4. The effector T cells are of the TH2 type, and the absence of lymphocyte infiltration retains the thyroid gland in operable condition. Therefore T3 and T4, no longer regulated by TSH, are secreted continuously in excess of concentrations required by the body.