ather than a unique disorder, Crohn's disease is regarded as a common denominator for various immune mediated inflammatory diseases of the gastrointestinal tract. These various subforms of Crohn's disease are characterised by T cell mediated tissue destruction in the gut. In contrast with autoimmune diseases where autoantibodies react with self antigens, inflammation in Crohn's disease is directed against antigens that are mainly derived from the environment. 1 Although it may sound trivial, this adjustment in the understanding of the pathogenetic mechanisms has a vast number of consequences for the search of the disease causing factors and identification of therapeutic targets.
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Gasché et al. (2004) studied this question.
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