Autoimmunity, as opposed to autoimmune disease, is vital to the development of a normal immune response. As we discussed previously, T cells recognise antigen only in association with self-MHC molecules; they will not respond if the antigen is presented by foreign MHC molecules, thus confirming that the reaction involves specific recognition of self molecules. This is an example of autoimmunity which is productive. A further example is the recognition of self-idiotypes by anti-idiotypic antibodies, which is essential for the diversification and regulation of immune responses. Apart from these instances, the immune system does not normally react to itself, i.e. it is tolerant to self.
Self-tolerance occurs early in foetal development and is vital for health and the normal functioning of the immune response; its breakdown resulting in autoimmune disease which may be debilitating or even fatal. How can such autoimmunity develop? One suggestion is that an antigen may be hidden from the immune system during development (e.g. an antigen within an organ which has little contact with immunologically active cells - an immunologically privileged site), thus preventing the development of tolerance to that antigen at the T or B cell level. If the antigen is exposed later in life as a result of some form of tissue damage, it will be foreign to the immune system and it will stimulate an (auto)immune response. This type of response may be a primary cause of, or a secondary complication in, a variety of human and animal diseases.
Many studies have demonstrated that self-reactive lymphocytes are part of the normal immunological repertoire and only a small fraction of these cells may be pathogenic; the remainder having a physiological role to play.
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