Clinicopathologic mechanisms in celiac disease

Abstract

The precise molecular immunogenetics of celiac disease continues to be defined. Susceptibility to celiac disease appears to be due to a particular HLA-DQ heterodimer and the association of the condition with HLA-DP is probably due to linkage disequilibrium. The role of small intestinal lymphocytes expressing the γ/Δ T-cell receptor in celiac disease continues to be investigated; their numbers are definitely raised in the condition but such increases are not restricted to celiac disease. The controversy surrounding the potential involvement of adenovirus 12 in the etiology of celiac disease is unresolved. Investigation continues into the precise structure of the peptide within gluten that is toxic.