Normal Incidence of Diabetes in NOD Mice Tolerant to Glutamic Acid Decarboxylase

Experiments in nonobese diabetic (NOD) mice that lacked expression of glutamic acid decarboxylase (GAD) in β cells have suggested that GAD represents an autoantigen essential for initiating and maintaining the diabetogenic immune response. Several attempts of inducing GAD-specific recessive tolerance to support this hypothesis have failed. Here we report on successful tolerance induction by expressing a modified form of GAD under control of the invariant chain promoter resulting in efficient epitope display. In spite of specific tolerance insulitis and diabetes occurred with normal kinetics indicating that GAD is not an essential autoantigen in the pathogenesis of diabetes.

• Publication year

  2003

• Venue

  Journal of Experimental Medicine

• Publication date

  2003-06-16

• Fields of study

  Biology, Medicine

• Identifiers
  DOI 10.1084/jem.20030215PMID 12796471PMCID 2193961
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

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