title: How specificity for self-peptides shapes the development and function of regulatory T cells.
abstract: The cataclysmic disease that develops in mice and humans lacking CD4+ T cells expressing the transcription factor Foxp3 has provided abundant evidence that Foxp3+CD4+ Tregs are required to suppress a latent autoreactivity of the immune system. There is also evidence for the existence of tissue-specific Tregs that can act to suppress regional autoimmune responses, suggesting that Tregs exert their effects, in part, through responding to self-peptides. However, how the immune system generates a repertoire of Tregs that is designed to recognize and direct regulatory function to self-peptides is incompletely understood. This review describes studies aimed at determining how T cell recognition of self-peptide(s) directs Treg formation in the thymus, including discussion of a modified "avidity" model of thymocyte development. Studies aimed at determining how TCR specificity contributes to the ability of Tregs to suppress autoimmune diseases are also discussed.
authors.affiliation: The Wistar Institute, Philadelphia, PA 19104, USA.
authors.forename: Donald M
authors.initials: DM
authors.lastname: Simons
authors.forename: Cristina Cozzo
authors.initials: CC
authors.lastname: Picca
authors.forename: Soyoung
authors.initials: S
authors.lastname: Oh
authors.forename: Olivia A
authors.initials: OA
authors.lastname: Perng
authors.forename: Malinda
authors.initials: M
authors.lastname: Aitken
authors.forename: Jan
authors.initials: J
authors.lastname: Erikson
authors.forename: Andrew J
authors.initials: AJ
authors.lastname: Caton
mesh_terms: D000818:Animals; D001324:Autoantigens / Q000276:immunology*; D001327:Autoimmune Diseases / Q000209:etiology / Q000276:immunology; D006801:Humans; D051379:Mice; D011948:Receptors, Antigen, T-Cell / Q000502:physiology; D050378:T-Lymphocytes, Regulatory / Q000502:physiology*; D013950:Thymus Gland / Q000502:physiology
chemical_list: D001324:Autoantigens; D011948:Receptors, Antigen, T-Cell