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Reversal of Sjögren’s-like syndrome in non-obese diabetic mice


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.

  • CFA, complete Freund’s adjuvant
  • FISH, fluorescence in situ hybridisation
  • LMP, latent membrane protein
  • MHC, major histocompatibility complex
  • NFκB, nuclear factor κB
  • NOD, non-obese diabetic
  • SFR, salivary flow rate
  • TNF, tumour necrosis factor

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