2012
DOI: 10.1016/j.lpm.2012.04.029
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Pathophysiological cytokine network in primary Sjögren's syndrome

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Cited by 15 publications
(7 citation statements)
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“…Notably, our observations that pancreatic protein-immunised mice did not exhibit any detectable immune responses and pathological changes in SG further confirm the antigen specificity against SG in ESS model. Earlier studies have suggested Th1 cytokine-mediated inflammatory responses in SS patients,33–36 but increasing evidence indicates the involvement of IL-17 in autoimmune inflammation during the pathogenesis of SS 37. Here, we reveal a significantly enhanced Th17 response occurring 7 days prior to the predominant Th1 response during ESS induction.…”
Section: Discussionsupporting
confidence: 46%
“…Notably, our observations that pancreatic protein-immunised mice did not exhibit any detectable immune responses and pathological changes in SG further confirm the antigen specificity against SG in ESS model. Earlier studies have suggested Th1 cytokine-mediated inflammatory responses in SS patients,33–36 but increasing evidence indicates the involvement of IL-17 in autoimmune inflammation during the pathogenesis of SS 37. Here, we reveal a significantly enhanced Th17 response occurring 7 days prior to the predominant Th1 response during ESS induction.…”
Section: Discussionsupporting
confidence: 46%
“…Th17 cells secrete IL‐17, which constitutes a family of cytokines that includes six members, from A to F, with a wide range of biological activities . Recent studies have demonstrated the involvement of IL‐17 in autoimmune inflammation during the pathogenesis of pSS and have revealed elevated levels of IL‐17A in body fluids from patients with pSS, including tears, saliva and serum . An analysis of mouse models showed that IL‐17‐deficient mice were completely resistant to ESS induction, and adoptive transfer of Th17 cells drove the development of ESS in IL‐17 KO mice .…”
Section: Discussionmentioning
confidence: 99%
“…SS is classified as either primary, when occurring alone, or secondary, when occurring along with another autoimmune diseases such as rheumatoid arthritis, systemic lupus erythematosus or myositis. Although the origin of the disease remains unknown, epithelial cell activation is considered to play a central role in the multifactorial pathogenesis of SS [ 67 , 68 , 69 , 70 ]. Several autoantibodies have been detected in patients suffering from SS and associated with clinical features of SS; including against ribonucleoproteins (Ro/SS-A) and La/SS-B), CA19-9, muscarinic M3 receptors and pancreatic ductal cells [ 71 , 72 , 73 , 74 ].…”
Section: Aquaporins and Pathophysiological Conditionsmentioning
confidence: 99%