[Interactions between enterocytes and lymphocytes in the pathogenesis of celiac disease]

Abstract

MHC antigens are positioned in the centre of the interactions between enterocytes and lymphocytes in the pathogenesis of coeliac disease. This disease is associated with the presence of specific alleles of MHC-class II genes. Class-II-gene products being present also on enterocytic membranes play an important role in the presentation of antigens and might lead in coeliac patients to an extraordinarily effective stimulation of CD4+ and/or CD8+ cells which induce damage to the intestinal epithelium by various mechanisms. Additionally so-called CD4-CD8-gamma/delta + lymphocytes might act cytotoxically on enterocytes. The typical HLA-haplotype, however, is found also in many healthy persons. Thus the presence of specific MHC molecules is not the only requirement for susceptibility to gliadins. Furthermore, a virus infection (cross reactivity with gliadins?) as an additional factor can not be considered to be sufficient for expression of coeliac disease. Results were presented demonstrating that gliadins affect undifferentiated enterocytes arguing for a role of additional enterocytic factors in the pathogenesis of the disorder. The findings suggest that gliadins interfere with late post-translational processes in the biosynthesis of sucrase-isomaltase. The integration of this effect into the pathogenetic mechanism of coeliac disease remains to be clarified.