Autoimmunity: Nursing

Autoimmunity is when the immune system perceives the body’s own cells or proteins as foreign antigens and triggers an immune response resulting in organ damage or systemic inflammation.

Let’s start by looking at how the body would normally prevent autoimmunity. Now, the immune response can be classified as innate and adaptive, and the latter is the main culprit with autoimmunity. See, the adaptive immune system is made up of B and T lymphocytes, also called B and T cells. Each lymphocyte only targets a specific pathogen, so you would have some lymphocytes that will only attack E. coli and some lymphocytes that only attack the influenza virus. This is called a specific immune response.

Now, the reason B and T cells can recognize specific pathogens is because each cell has B or T cell receptors that only bind to a specific antigen, and they need to come in contact with one of these antigens in order to activate. Usually, an antigen presenting cell, or an APC, like a macrophage or dendritic cell brings the antigen to the lymphocytes and causes them to activate. This will cause clonal expansion, meaning the activated lymphocyte will quickly proliferate, creating an army of lymphocytes that also targets the same antigen. If the lymphocyte is a B cell, it will start creating antibodies against the antigen. If the lymphocyte is a T helper cell, it can help activate other lymphocytes like B cells, or it could call cells like macrophages and neutrophils to the pathogen to destroy it.

Now, the B and T cell receptors are generated randomly, but there are so many lymphocytes in the body that it’s likely some will target whatever pathogen enters the body. The downside is this random process inevitably leads to lymphocytes with receptors to self antigens. To ensure these lymphocytes do not attack other healthy cells in the body, there are processes called central and peripheral tolerance.

In central tolerance, APCs constantly bring different self peptides to immature T cells in the thymus and immature B cells in the bone marrow. If the immature lymphocyte binds to the self peptide strongly, they undergo apoptosis where they self-destruct, and this is called clonal deletion. In peripheral tolerance, surviving T and B cells are tested again after they leave the thymus and bone marrow and any self reactive lymphocytes that escaped central tolerance will either undergo apoptosis or anergy where they’re basically turned off and can no longer respond to antigens. This process is assisted by a special type of T cell called regulatory T cells which also play a role in suppressing immune responses.

Now, the exact cause of autoimmune diseases is unknown, but it's believed to be associated with certain risk factors. Modifiable risk factors include various medications, like procainamide and hydralazine, whereas nonmodifiable risk factors include being assigned female at birth, age over 50, personal or family history of autoimmune disease, as well as hormonal changes during major endocrinological transition, like puberty and menopause. For example, symptoms of autoimmune diseases tend to improve during pregnancy, but get even worse after delivery.