To remove T cells that have high affinity for “self” antigens and facilitate the development of nTregs, peripheral tissue-specific antigens under the control of a transcriptional regulator (autoimmune regulator; AIRE) are presented on MHC molecules by medullary thymic epithelial cells (mTECs) to developing thymocytes (135, 136); mutations in the gene encoding AIRE result in autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy (APECED), a multiorgan autoimmune disorder caused by the release of “self” reactive T cells into the periphery (137). This evidence concerns the gene AIRE and autoimmune polyendocrine syndrome type 1.