Abstract
The incidence of some autoimmune diseases is increasing dramatically in the developed world. For example, the incidence of the autoimmune disease, Type 1 diabetes (T1D), is increasing in the UK at a rate of 4% per annum; faster than can be accounted for by genetic change. In the case of T1D, as for many autoimmune diseases, the development of the disease is known to have a genetic component with many genes playing a role in governing the development of disease [1]. However, the development of Type 1 diabetes is not wholly governed by genetics and a role for environmental factors is shown by the 40% concordance rate for development of T1D in identical twins. This lack of 100% concordance in identical twins which is indicative of environmental effects acting on a genetic background is also seen for some other autoimmune diseases such as multiple sclerosis (MS) and systemic lupus erythematosus (SLE). There has been considerable interest in analysing the basis for the dramatic rise in incidence of T1D in the developed world with particular emphasis being placed on the role that infection might play in exacerbating or preventing onset of this autoimmune condition. The evidence that infection may play a role in the prevention of T1D is discussed in this chapter. KeywordsMultiple SclerosisSystemic Lupus ErythematosusExperimental Autoimmune EncephalomyelitisPancreatic Beta CelliNKT CellThese keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.
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