Celiac disease is the major nutrient-induced disease of the small intestine. The disease is traditionally characterized by villous atrophy responsive to gliadin. Recent data suggest that there is an extended spectrum of gluten sensitivity that includes first-degree relatives and patients with latent celiac disease. Genetic studies have identified HLA DQ A1 *0501 B1 *0201 as the predominant HLA gene most tightly linked to this condition. Gliadin-specific T cell clones restricted by DQ have now been identified in the small intestine lamina propria. Such T cells may be important in mediating many of the features of the disease. This review discusses the interrelationship of genetics, cereal chemistry, environmental factors, and immunology involved in the pathogenesis of celiac disease and explores its relationship with other nutrient-induced enteropathies.