Abstract
Autoimmune disease results from an inability of the immune system to differentiate self-antigens from those of a foreign and harmful organism. Since the immune system is forced to deal with an unforeseeable variety of pathogens, it is impossible to design an effective immune system that is incapable of reacting against self-antigens. Instead, a complex system of checks and balances has evolved to keep the immune system from reacting harmfully against “self.” Accordingly, while autoimmune T cells and B cells may well be part of the healthy immune system, as often are autoantibodies, a failure to repress these cells results in the activation of the immune system’s effector mechanisms. This will almost always lead to inflammation and damage, that is, autoimmune disease. In the absence of a reliable way of specifically removing autoimmune cells, most successful clinical strategies target the effector mechanisms in the treatment of autoimmunity. It is therefore important to understand these effector mechanisms and to both recognize their role in autoimmune diseases and minimize their harmful effects.
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