autoimmune endocrine disease
The immune system is supposed to attack invaders and leave the body's own tissues alone. In autoimmune endocrine disease, that recognition fails and the immune system turns on a hormone-producing gland as if it were foreign. It is friendly fire aimed at an endocrine organ, and the result depends on what the attack does to the gland.
Sometimes the attack destroys the gland, causing hormone deficiency: this is how type 1 diabetes erases the insulin-making beta cells, how Hashimoto's thyroiditis gradually wipes out thyroid tissue, and how autoimmune Addison's disease ruins the adrenal cortex. Other times the immune attack mimics a hormone signal rather than destroying tissue: in Graves' disease, antibodies bind the TSH receptor and switch the thyroid on, producing hormone excess instead. The same self-targeting process can thus cause either too little or too much hormone.
These diseases tend to run in families and to cluster together, because shared genetic tendencies toward autoimmunity affect more than one gland. Doctors often detect them by finding specific autoantibodies — proteins the immune system has made against gland components — long before, or alongside, the gland's failure. Treatment usually addresses the resulting hormone problem (replacing what is lost or blocking what is excess) rather than curing the underlying immune attack.
Type 1 diabetes is an autoimmune endocrine disease in which immune cells destroy pancreatic beta cells; autoantibodies can often be detected in the blood before blood sugar ever rises.
Antibodies can precede the gland's failure.
Whether autoimmunity causes deficiency or excess depends on the antibody's effect: destroying or blocking antibodies cause underfunction, while stimulating antibodies that activate a receptor cause overfunction, as in Graves' disease.