Abstract
Autoimmune and allergic diseases occur when an individual mounts an inappropriate immune response to a self-antigen or an innocuous environmental antigen. This triggers a pathogenic T-cell response resulting in damage to specific tissues and organs. In type 1 diabetes (T1D), this manifests as destruction of the insulin-secreting β cells, resulting in a life-long dependency on recombinant insulin. Modulation of the pathogenic T-cell response with antigen-specific peptide immunotherapy offers the potential to restore the immune homeostasis and prevent further tissue destruction. Recent clinical advances with peptide therapy approaches in both T1D and other diseases are beginning to show encouraging results. New technologies targeting the peptides to specific cell types are also moving from pre-clinical development to the clinic. While many challenges remain in clinical development, not least selection of the optimal dose and dosing frequency, this is clearly becoming a very active field of drug development.
Highlights
Type 1 diabetes (T1D) is an organ-specific autoimmune disease
While there have been significant advances in recombinant human insulins and technologies both to deliver insulin and monitor blood glucose levels, many patients do not achieve optimal glycemic control. This is apparent in children and young adults, in whom blood glucose control, measured by glycated hemoglobin (HbA1c) levels, is typically poor, reaching greater than 8% in the majority when the desired levels are below 7.5% [1]
There is a need for new therapies that either preserve or restore β-cell function to improve glycemic control and patient outcomes
Summary
Type 1 diabetes (T1D) is an organ-specific autoimmune disease. Auto-reactive T cells attack the insulin-producing beta (β) cells of the pancreatic islets, leading to a loss of endogenous insulin production and subsequent impaired glucose metabolism. While there have been significant advances in recombinant human insulins and technologies both to deliver insulin and monitor blood glucose levels, many patients do not achieve optimal glycemic control. This is apparent in children and young adults, in whom blood glucose control, measured by glycated hemoglobin (HbA1c) levels, is typically poor, reaching greater than 8% in the majority when the desired levels are below 7.5% [1]. There are supportive data to suggest that preservation of residual β-cell function at the time of diagnosis may lead to improvements in glycemic control [3, 4] and thereby impact upon long-term outcomes. Preventing immune-mediated attack on β cells would open the possibility for β-cell regeneration and/or replacement therapies to be more effective and durable
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