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BioMed Research International
Volume 2017 (2017), Article ID 5981432, 6 pages
Research Article

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

1Department of Rheumatology and Clinical Immunology, The First Hospital of Xiamen University, Xiamen 361003, China
2Xiamen Key Laboratory of Rheumatology and Clinical Immunology, Xiamen, China
3The Chenggong Hospital Affiliated to Xiamen University, Xiamen, Fujian, China

Correspondence should be addressed to Yan He and Guixiu Shi

Received 26 October 2016; Accepted 6 February 2017; Published 23 February 2017

Academic Editor: Xiaoquan Rao

Copyright © 2017 Jiao Luo et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


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.