An autoimmunized mouse model recapitulates key features in the pathogenesis of Sjugren's syndrome

Xiang Lin, Ju-xian Song, Pang-Chui Shaw, Tzi-Bun Ng, Stephen Cho-Wing Sze, Yao Tong, Kai-Fai Lee, Kalin Yanbo Zhang*

*Corresponding author for this work

Research output: Contribution to journalJournal articlepeer-review

21 Citations (Scopus)


The pathogenesis of Sjögren’s syndrome (SS) is poorly understood. To evaluate an autoimmunization-induced experimental SS model, we firstly observed the phenotype of lymphocyte infiltration in the enlarged submandibular gland (SG). Furthermore, significant activation of caspase-3 and a high ratio of Bax-to-Bcl-2 were detected, indicating the inflammatory apoptosis associated with developmental foci. Meanwhile, the dysregulated cytokines, such as tumor necrosis factor α, IL-1β and IL-6 mRNA expression, were found to be over-expressed. A progressive decrease of aquaporin 5 and its subcellular translocation from apical to basal membrane in SG was found to be associated with the abnormally expressed M3 muscarinic acetylcholine receptor. This pattern was found to be similar to that seen in human SS and possibly contributed to the saliva secretion deficiency. Thus, this autoimmunization-induced model recapitulates the key features of human SS and may have potential for studying the pathogenesis of human SS.
Original languageEnglish
Pages (from-to)613-624
Number of pages12
JournalInternational Immunology
Issue number10
Early online date16 Aug 2011
Publication statusPublished - Oct 2011

Scopus Subject Areas

  • Immunology and Allergy

User-Defined Keywords

  • apoptosis
  • aquaporin 5
  • mouse model
  • M3 mucarinic acetylcholine receptor
  • Sjögren’s syndrome


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