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The external world of gluten and autoimmunity
  1. M LONDEI
  1. Kennedy Institute of Rheumatology Division
  2. Imperial College School of Medicine
  3. 1 Aspenlea Road, London W6 8LH, UK
  4. m.londei@ic.ac.uk

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This commentary is not about autoimmune diseases, and therefore I will not discuss why a significant proportion of individuals are prone to develop autoimmune diseases. Suffice to say that this failure to spare self might represent an advantage when fighting infections. In autoimmunity there is a clear genetic involvement with a strong association between these diseases and some HLA alleles,1but autoimmunity is not simply genetically controlled and environmental factors are essential. For example, in the syngenic NOD mice, the preferred animal model for type 1 diabetes, simple modifications in the “cleanness” of the housing conditions dramatically changes the incidence of the disease.2 More poignantly, in the context of a clinical setting, the concordance rate of autoimmune diseases in monozygous (genetically identical) twins is less than 50%.3 Hence environmental factor(s) are essential in induction of autoimmunity. Thus characterisation of “environmental” triggers and how they might promote autoimmunity is of paramount importance if we wish to understand, prevent, and eventually define strategies to treat these diseases. The gastrointestinal tract, with its vast surface of contact with the external world, represents the main door for the potential encounter of “environmental” triggers of autoimmunity.

To curb this risk, the gastrointestinal tract, as other mucosae, has devised means of inducing a protective response that however lacks the inflammatory flavour. In a simplistic way, antigens encountered on a mucosal surface trigger a Th2 (sometimes and depending on the authors Th3 or T regulatory) type of response instead of a proinflammatory Th1 …

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