A Potential of sFasL in Preventing Gland Injury in Sjogren’s Syndrome

Fas and its ligand FasL, members of tumor necrosis factor receptor superfamily, have been implicated in the process of cell apoptosis. FasL consists of two forms, membrane FasL (mFasL) and soluble FasL (sFasL). sFasL can be produced by mFasL cleaved by matrix metalloproteinases (MMP) and also reveal...

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Published inBioMed research international Vol. 2017; no. 2017; pp. 1 - 6
Main Authors He, Yan, Qian, Hongyan, Yu, Bing, Wang, Ying, Luo, Jiao, Shi, Guixiu
Format Journal Article
LanguageEnglish
Published Cairo, Egypt Hindawi Publishing Corporation 01.01.2017
Hindawi
John Wiley & Sons, Inc
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ISSN2314-6133
2314-6141
2314-6141
DOI10.1155/2017/5981432

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Summary:Fas and its ligand FasL, members of tumor necrosis factor receptor superfamily, have been implicated in the process of cell apoptosis. FasL consists of two forms, membrane FasL (mFasL) and soluble FasL (sFasL). sFasL can be produced by mFasL cleaved by matrix metalloproteinases (MMP) and also reveals a role for binding to Fas which is expressed on cell surface. Although Fas/FasL axis has been implicated in a variety of diseases, its role in Sjogren’s syndrome still remains ill defined. In this study, we investigated the potential of sFasL in the pathogenesis of Sjogren’s syndrome (SS). We found that the serum levels of sFasL in SS patients were significantly lower than healthy subjects. Moreover, serum levels of sFasL in patients with mild disease activity were higher than patients with severe disease activity. There is a positive correlation of the serum level of sFasL with uptake index of parotid gland in our expectation. In addition, liver injury involvement in SS patients showed decreased level of sFasL. Furthermore, we here also observed that the protective cytokine IL-10 expression was positively correlated with sFasL expression. Thus, our results here suggest a potential of sFasL in maintaining gland organ homeostasis.
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Academic Editor: Xiaoquan Rao
ISSN:2314-6133
2314-6141
2314-6141
DOI:10.1155/2017/5981432