title: β-Cell differentiation and regeneration in type 1 diabetes.
abstract: Pancreatic insulin-producing β-cells have traditionally been viewed as a quiescent cell population. However, several recent lines of evidence indicated that like most tissues the β-cell mass is dynamically regulated with ongoing β-cell regeneration throughout life to replenish lost or damaged β-cells. In type 1 diabetes (T1D), this fine-tuned balance between β-cell death and β-cell renewal in the endocrine pancreas is lost and the deficit in β-cell mass is largely caused by autoimmune-mediated apoptosis. Currently, the concept that a cure for T1D will require both re-establishment of immunological tolerance along with replacement or regeneration of a functional β-cell mass in T1D patients is generally accepted. In this study our current understanding of the events directing β-cell replication, β-cell reprogramming from different cell types and β-cell regeneration is reviewed, in view of the results of various immunomodulatory strategies aiming at blocking autoimmune responses against pancreatic β-cells and at improving β-cell mass and function in subjects with T1D.
authors.affiliation: Laboratory of Clinical and Experimental Endocrinology, Campus Gasthuisberg O&N1, Faculty of Medicine, Katholieke Universiteit Leuven, Leuven, Belgium.
authors.forename: L
authors.initials: L
authors.lastname: Ding
authors.forename: C
authors.initials: C
authors.lastname: Gysemans
authors.forename: C
authors.initials: C
authors.lastname: Mathieu
mesh_terms: D000818:Animals; D002454:Cell Differentiation; D049109:Cell Proliferation; D054338:Cell Transdifferentiation / Q000502:physiology; D003922:Diabetes Mellitus, Type 1 / Q000473:pathology / Q000503:physiopathology*; D006801:Humans; D050417:Insulin-Secreting Cells / Q000473:pathology / Q000502:physiology*; D007515:Islets of Langerhans / Q000473:pathology / Q000502:physiology; D012038:Regeneration / Q000502:physiology*
keywords: regeneration; replication; reprogramming; type 1 diabetes; β-cells