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Molecular Interactions Governing Autoantigen Presentation in Type 1 Diabetes

Journal

CURRENT DIABETES REPORTS
Volume 15, Issue 12, Pages -

Publisher

CURRENT MEDICINE GROUP
DOI: 10.1007/s11892-015-0689-z

Keywords

Diabetes; Autoimmunity; HLA; Insulin; T cells

Funding

  1. National Institute of Diabetes and Digestive Kidney Diseases [R01DK099317, K08 DK095995]
  2. Juvenile Diabetes Research Foundation
  3. Children's Diabetes Foundation

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Type 1 diabetes is a chronic autoimmune disease resulting from T cell-mediated destruction of insulin-producing beta cells within pancreatic islets. Disease incidence has increased significantly in the last two decades, especially in young children. Type 1 diabetes is now predictable in humans with the measurement of serum islet autoantibodies directed against insulin and beta cell proteins. Knowledge regarding the presentation of insulin and islet antigens to T cells has increased dramatically over the last several years. Here, we review the trimolecular complex in diabetes, which consists of a major histocompatibility molecule, self-peptide, and T cell receptor, with a focus on insulin peptide presentation to T cells. With this increased understanding of how antigens are presented to T cells comes the hope for improved therapies for type 1 diabetes prevention.

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