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The Autoimmune Mechanism in Graves' Disease

© Elaine Moore

While genetic and environmental factors are ultimately responsible for autoimmune disease development, the interactions between the immune system, the nervous system and the endocrine system are essential for the full blown immune response that leads to the development of autoimmune endocrine disease.

Current evidence indicates that lymphocyte proliferation, which is the prerequisite for the immune reaction that leads to autoimmunity, is regulated by hormones, adhesion molecules, cytokines and neuropeptides and neurotransmitters secreted by neuroendocrine cells. Adhesion molecules and cytokines are chemical molecules released during the immune response. These chemicals can act as messengers causing or inhibiting various growth factors and they can initiate secondary steps leading to the production of autoantibodies. Neuropeptides and neurotransmitters are chemical molecules such as the endorphins and serotonin, which have hormone-like properties.

During systemic infectious disease, severe autoimmune reactions, trauma, or shock, excess amounts of cytokines re released, initiating a rapid neuroendocrine and metabolic response known as the acute phase response. In this condition, the nonspecific immune defense of the body is significantly elevated (antibody production) while classical immune reactions are suppressed (suppressor T cell activity is diminished). These are the mechanisms behind autoimmune thyroid disorders.

Autoimmune disease is the result of disturbed immunoregulation leading to the breakdown of self-tolerance (normally the immune system does not react to self components, this is known as self-tolerance). This allows the proliferation and differentiation of autoreactive lymphocyte clones, which in turn cause autoantibody development and autoimmune disease.

The underlying defects that play a role in the development of autoimmune disease may lie in the endocrine system, in cell-to-cell communication, and in cytokine-mediated regulations. It’s likely that more than one regulatory defect is required for the development of full blown autoimmune disease. For instance, while iodine supplementation is known to trigger autoimmune thyroid disease in susceptible individuals, a defect in the iodide symporter pump causes this susceptibility to iodine (Jod-Basedow effect). And while infectious agents trigger many different autoimmune diseases, it’s a defect in cytokine regulations and cell to cell communications that causes the immune system to err when it initiates an assault on self-antigens.

Furthermore, the role of environmental factors such as stress in autoimmune disease development stems from direct effect on neuroendocrine cells. In chronic stress, neuroendocrine cells release neurotransmitters and neuropeptides that signal immune system cells to protect us by slowing down and allowing the body to prepare for death. Natural Killer cells and suppressor lymphocytes that normally would prevent autoimmune disease are diminished.