Dataset Information
Reversal of Sjogren's-like syndrome in non-obese diabetic mice.
Ontology highlight
ABSTRACT: Background
Non-obese diabetic (NOD) mice exhibit autoimmune diabetes and Sjögren's-like syndrome.Objective
To test whether a treatment that reverses end-stage diabetes in the NOD mouse would affect their Sjögren's-like syndrome.Methods
NOD mice have a proteasome defect. Improperly selected naive T cells escape, but can be killed by reintroducing major histocompatibility complex class I self-peptides on matched normal splenocytes. The proteasome defect also impairs nuclear factor kB, a transcription factor in pathogenic memory T cells, increasing their susceptibility to tumour necrosis factor-induced apoptosis stimulated through complete Freund's adjuvant (CFA). The impact of this two-limb therapy (injections of matched normal splenocytes and CFA) on the autoimmune salivary gland disease of the NOD mice was studied.Results
All NOD mice receiving the above treatment had a complete recovery of salivary flow and were protected from diabetes. Restoration of salivary flow could be the result of a combination of rescue and regeneration of the gland, as confirmed by immunohistochemical analysis. All untreated NOD mice showed a continuous decline in salivary flow, followed by hyperglycaemia and death.Conclusion
This study establishes that a brief intervention in NOD mice with Sjögren's-like syndrome can reverse salivary gland dysfunction.
SUBMITTER: Tran SD
PROVIDER: S-EPMC1954678 | biostudies-literature | 2007 Jun
REPOSITORIES: biostudies-literature
Publications
Reversal of Sjogren's-like syndrome in non-obese diabetic mice.
Annals of the rheumatic diseases 20061219 6
<h4>Background</h4>Non-obese diabetic (NOD) mice exhibit autoimmune diabetes and Sjögren's-like syndrome.<h4>Objective</h4>To test whether a treatment that reverses end-stage diabetes in the NOD mouse would affect their Sjögren's-like syndrome.<h4>Methods</h4>NOD mice have a proteasome defect. Improperly selected naive T cells escape, but can be killed by reintroducing major histocompatibility complex class I self-peptides on matched normal splenocytes. The proteasome defect also impairs nuclear ...[more]
