Coeliac disease is a permanent intolerance to wheat gliadins and related pr
olamines. patients who have an obvious malabsorption syndrome form only a s
mall minority of the total number of people with coeliac disease. There are
, in fact, no pathognomonic clinical features, and the condition is defined
and diagnosed by the presence of pathological changes in the small bowel m
ucosa related to the presence of toxic prolamines. Susceptibility to coelia
c disease is determined to a significant extent by genetic factors. A large
part of the genetic susceptibility maps to the HLA region on chromosome 6,
us approximately, 95% of coeliac disease patients carry an almost identica
l HLA DQ2/heterodimer; a role of non-HLA genes has also been postulated. Fr
om a pathogenetic point of view: most evidence supports the notion of a De-
restricted gluten-specific Th1 response in the lamina propria; nonetheless,
it is possible that, in coeliac subjects, gluten, prior to T cell activati
on, could exert a direct toxic effect leading to the production of proinfla
mmatory signals.