Abstract
The immune system is programmed to defend the body against invading microbes by recognising antigens displayed on the surface of the organisms. At the same time, the immune system should not respond to “self” antigens. This ability to discriminate between “foreign” and “self” is known as immunological tolerance. Autoimmune disease develops when “tolerance” to self antigens breaks down. Currently, little is known about how tolerance can be broken, although it is generally thought that this may occur in genetically susceptible individuals exposed to certain environmental “triggers”. Furthermore, little is known about the early events which initiate the immune response to self antigens and in particular the way in which self antigens are recognised by T cells to activate the self-destructive autoimmune process. While in full blown autoimmune disease, the autoimmune response is clearly recognising a number of different antigenic determinants, it is possible that the early response may be directed towards one or only a few antigenic determinants.
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© 1994 Springer-Verlag Berlin Heidelberg
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Gleeson, P.A., Toh, BH., Alderuccio, F., van Driel, I.R. (1994). The Gastric H/K-ATPase: The Principle Target in Autoimmune Gastritis. In: Hirst, B.H. (eds) Molecular and Cellular Mechanisms of H+ Transport. NATO ASI Series, vol 89. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-79301-1_14
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DOI: https://doi.org/10.1007/978-3-642-79301-1_14
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