摘要
Type 1 diabetes is characterized by recognition of one or more beta-cell proteins by the immune system. The list of target antigens in this disease is ever increasing and it is conceivable that additional islet autoantigens, possibly including pivotal beta-cell targets, remain to be discovered. Many knowledge gaps remain with respect to the disorder%26apos;s pathogenesis, including the cause of loss of tolerance to islet autoantigens and an explanation as to why targeting of proteins with a distribution of expression beyond beta cells may result in selective beta-cell destruction and type 1 diabetes. Yet, our knowledge of beta-cell autoantigens has already led to translation into tissue-specific immune intervention strategies that are currently being assessed in clinical trials for their efficacy to halt or delay disease progression to type 1 diabetes, as well as to reverse type 1 diabetes. Here we will discuss recently gained insights into the identity, biology, structure, and presentation of islet antigens in relation to disease heterogeneity and beta-cell destruction.
- 出版日期2012-4