Type 1 diabetes (T1D) results from an autoimmune destruction of the insulin-producing beta
cells. The process of autoimmune destruction 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. Evidence is now emerging in humans that these approaches may be effective in
chronic inflammatory diseases such as multiple sclerosis and allergy. Administration of oral
insulin in multiple islet autoantibody-positive children offers the potential for inducing
immunological tolerance to beta cells and thereby protect against further development
progression to type 1 diabetes.
Phase:
Phase 2
Details
Lead Sponsor:
Technische Universität München
Collaborators:
Helmholtz Zentrum München Ludwig-Maximilians - University of Munich Technische Universität Dresden The Leona M. and Harry B. Helmsley Charitable Trust