title: The APC1 concept of type I diabetes.
abstract: Type I diabetes appears to be a T cell dependent disease. T cell reactivity is regulated by antigen presenting cells (APCs). In animal models of type I diabetes, abnormal reactivity of APCs, in particular of macrophages, probably is responsible for the progression of islet inflammation from T helper type 2 dependent benign periinsulitis to T helper type I dependent destructive intrainsulitis. The functional state of APCs during preferential stimulation of Th1 reactivities (APC1 state) is characterized by the release of TNFalpha, IL-12 and/or IL-18. The bias towards APC1 reactivity has been found due to defective inhibition via IL-10 and PGE2.
authors.affiliation: Diabetes Research Institute at the Heinrich-Heine University of Düsseldorf, Germany.
authors.forename: H
authors.initials: H
authors.lastname: Rothe
authors.forename: H
authors.initials: H
authors.lastname: Kolb
mesh_terms: D000818:Animals; D000938:Antigen-Presenting Cells / Q000276:immunology*; D015551:Autoimmunity; D016207:Cytokines / Q000096:biosynthesis; D003922:Diabetes Mellitus, Type 1 / Q000209:etiology / Q000276:immunology*; D015232:Dinoprostone / Q000096:biosynthesis; D006801:Humans; D007378:Interleukins / Q000096:biosynthesis; D008264:Macrophages / Q000276:immunology; D051379:Mice; D016688:Mice, Inbred NOD; D008954:Models, Biological; D018417:Th1 Cells / Q000276:immunology; D018418:Th2 Cells / Q000276:immunology; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis
chemical_list: D016207:Cytokines; D007378:Interleukins; D014409:Tumor Necrosis Factor-alpha; D015232:Dinoprostone