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Vaccines for type 1 diabetes in the late stage of clinical development

Indian Journal of Pharmacology
Medknow Publications
Publication Date
DOI: 10.4103/0253-7613.83130
  • Letters To The Editor
  • Biology
  • Medicine


Sir, Type 1 diabetes results from autoimmune destruction of insulin-producing beta cells in the pancreatic islets of Langerhans. Recent advances in the understanding of the autoimmune process leading to diabetes have generated interest in the potential use of vaccines to prevent type 1 diabetes. Vaccines may act by various ways, including changing the immune response from proinflammatory T-helper-1 (Th1) phenotype to an anti-inflammatory T-helper-2 (Th2) phenotype. This Th1-Th2 shift occurs via a change in the type of cytokine signaling molecules being released by regulatory T-cells. Instead of pro-inflammatory cytokines, the regulatory T-cells begin to release cytokines that inhibit inflammation. This phenomenon is known as “acquired immune tolerance”. Autoantigens are being tried to induce immunologic tolerance. Several autoantigens have been identified in patients with type 1 diabetes such as glutamic acid decarboxylase (GAD) 65 and heat shock protein (HSP) 60.[1] Promising vaccination intervention based on GAD65 and HSP60 autoantigens are in late stage of clinical development. Vaccine based on GAD65 GAD65 vaccine comprises alum-formulated glutamic acid decarboxylase (GAD-65), a major auto-antigen in Type 1 diabetes. Studies on non obese diabetic (NOD) mice have indicated that GAD65 prevents type 1 diabetes. Prevention of the diabetes was mediated by the induction of GAD65-specific CD4+ regulatory T-cells and it was found that these CD4+ regulatory T-cells had a T-helper 2 phenotype.[2] The efficacy and safety of alum-formulated GAD65 (GAD65-alum) to reverse recent-onset type 1 diabetes in children and adolescents was assessed in a randomized, placebo-controlled phase II study. Seventy patients with recent-onset type 1 diabetes who had fasting C-peptide levels above 0.1 nmol per liter (0.3 ng per milliliter) and GAD autoantibodies were randomly assigned to receive subcutaneous injections of 20 μg of GAD-alum (35 patients) or placebo (alum alone, 35 patients) on study days 1 and 30

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