Infection and Autoimmune Thyroid Disease

Open Access
Publisher Website
Google Scholar
Abstract
In many different ways, it is difficult to tolerate oneself. But if we fail, autoimmune disease may develop. Immunologically speaking, the body has a number of ways to recognize external danger, and this results in a fierce immune attack on the culprits. These reactions, however, may sometimes go astray and damage not only the external cause of the danger, such as bacteria, but also the endogenous standby—oneself. Luckily, or by design, depending on your point of view, there are multiple controls to help us tolerate ourselves and prevent self-immolation, and only when these systems fail do we develop autoimmune disease. Elimination, via apoptosis, of T and B cells with a high avidity to self is the overall goal that has to be maintained throughout life. This may occur centrally in the thymus (1), where almost all self-antigens can be found at low levels, or peripherally at the site where self-antigens are normally expressed. Any T and B cells that escape early removal are kept suppressed by specific T regulatory cells (2). Some of us are more apt to develop autoimmune reactions than others, and much has been written about the role of genetics and the environment in the susceptibility and subsequent development of these complex disorders.