ABSTRACT
Increased frequencies of association of celiac disease with “autoimmune diseases” have been reported and reviewed extensively. Some understanding of the pathogenic significance of IgA-endomysial antibodies (EmA) derives from the nature and distribution of the antigens with which they react. Current studies on autoimmunity frequently focus on the role of T helper cells and T suppressor cells in the induction of autoimmunity. The role of genetic factors in the susceptibility to celiac disease is demonstrated most clearly by the fact that documented cases of the disease are very rare or nonexistent among Africans, Chinese, or Japanese. Alterations in antigen processing are implicated by the observation that there appears to be a direct cause-and-effect relationship between the intake of gluten by patients with gluten-sensitive enteropathy and their development, first of antigliadin antibodies and then of the specific autoantibodies IgA-EmA and IgA-Antireticulin antibodies, followed by the appearance of demonstrable villous atrophy.
