LAUSR

Type 1 diabetes (T1D) is a chronic disease caused by the destruction of pancreatic β cells, which is driven by autoreactive T lymphocytes. It has been described that a high proportion of T1D patients develop other autoimmune diseases (AIDs), such as autoimmune thyroid disease, celiac disease, or vitiligo, which suggests the existence of common etiological factors among these disorders. In this regard, genetic studies have identified a high number of loci consistently associated with T1D that also represent established genetic risk factors for other AIDs. In addition, studies focused on identifying the shared genetic component in autoimmunity have described several common susceptibility loci with a potential role in T1D. Elucidation of this genetic overlap has been useful in identifying key molecular pathways with a pathogenic role in multiple disorders. In this review, we summarized recent advances in understanding the shared genetic component between T1D and other AIDs and discuss how the identification of common pathogenic mechanisms can help in the development of new therapeutic approaches as well as in improving the use of existing drugs.