title: Does the gut microbiota have a role in type 1 diabetes? Early evidence from humans and animal models of the disease.
abstract: Despite years of appreciating the potential role of environment to influence the pathogenesis of type 1 diabetes, specific agents or mechanisms serving in such a capacity remain ill defined. This is exceedingly disappointing as the identification of factors capable of modulating the disease, either as triggers or regulators of the autoimmune response underlying type 1 diabetes, would not only provide clues as to why the disorder develops but, in addition, afford opportunities for improved biomarkers of disease activity and the potential to design novel therapeutics capable of disease abatement. Recent improvements in sequencing technologies, combined with increasing appreciation of the role of innate and mucosal immunity in human disease, have stirred strong interest in what is commonly referred to as the 'gut microbiota'. The gut (or intestinal) microbiota is an exceedingly complex microenvironment that is intimately linked with the immune system, including the regulation of immune responses. After evaluating evidence supporting a role for environment in type 1 diabetes, this review will convey current notions for contributions of the gut microbiota to human health and disease, including information gleaned from studies of humans and animal models for this autoimmune disorder.
authors.affiliation: Department of Pathology, University of Florida, College of Medicine, 1600 SW Archer Road, Gainesville, FL 32610-0275, USA. atkinson@ufl.edu
authors.forename: M A
authors.initials: MA
authors.lastname: Atkinson
authors.forename: A
authors.initials: A
authors.lastname: Chervonsky
mesh_terms: D000818:Animals; D003922:Diabetes Mellitus, Type 1 / Q000276:immunology* / Q000382:microbiology* / Q000503:physiopathology; D004195:Disease Models, Animal; D006801:Humans; D007113:Immunity, Innate / Q000502:physiology*; D007422:Intestines / Q000276:immunology / Q000382:microbiology*; D054892:Metagenome / Q000502:physiology*