Celiac disease is predominately a T cell-mediated immune disease caused by sensitivity to the dietary protein gluten. It is primarily a disease of Caucasians, with a population prevalence of approximately 1%[1]–[3]. The role of the major histocompatibility complex (MHC) in celiac disease was first reported 30 years ago [4], [5], with the identification of HLA-DQ2 almost 20 years ago [6]. At least 35% of the disease risk can be attributed to the necessary high-risk HLA types. However, the HLA high-risk genotypes are not sufficient to cause celiac disease. Genome-wide association studies (GWAS) and follow-up studies have identified 40 non-HLA loci that are associated with celiac disease, that combined explain approximately 5% of the disease risk [7]–[11], leaving most of the risk unexplained. In this study of North American celiac disease cases, we conducted a GWAS to identify additional loci and to confirm suspected loci. In addition, at the identified loci, we tested the association of the celiac loci with dermatitis herpetiformis and microscopic colitis. Dermatitis herpetiformis is regarded as an alternative phenotypic expression of gluten-sensitive enteropathy, with little known about
