Type 1 diabetes (T1D) results from an autoimmune destruction of the insulin-producing beta
cells within the pancreatic islets of Langerhans. This process is identified by circulating
islet autoantibodies to beta cell antigens, and is mediated by a lack of immunological
self-tolerance. Self-tolerance is achieved by T cell exposure to antigen in the thymus or
periphery in a manner that deletes autoreactive effector T cells or induces regulatory T
cells. Immunological tolerance can be achieved by administration of antigen under appropriate
conditions. Administration of oral insulin in islet autoantibody-negative children who are
genetically predisposed for T1D offers the potential for inducing immunological tolerance to
beta cells and thereby protect against the development of islet autoimmunity and T1D.
Phase:
Phase 2
Details
Lead Sponsor:
Technische Universität München
Collaborators:
German Center for Diabetes Research Helmholtz Zentrum München Ludwig-Maximilians - University of Munich Technische Universität Dresden