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Clinical and Experimental Medicine

Erschienen in:

11.12.2015 | Original Article

X-linked ectodermal dysplasia receptor (XEDAR) gene silencing prevents caspase-3-mediated apoptosis in Sjögren’s syndrome

verfasst von: Margherita Sisto, Loredana Lorusso, Sabrina Lisi

Erschienen in: Clinical and Experimental Medicine | Ausgabe 1/2017

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Abstract

Despite recent advancements in the knowledge of the etiology and pathogenic mechanisms, treatment of the autoimmune disease Sjögren’s syndrome (SS) remains mostly empiric and symptom-based, indicating the need for novel therapeutic approaches. Ectodysplasin-A2 (EDA-A2) is a recently isolated member of the tumor necrosis factor superfamily that binds to X-linked ectodermal dysplasia receptor (XEDAR). In this report, we have analyzed the expression and the biological activity of EDA-A2 in human salivary gland epithelial cells (SGEC) from primary Sjögren’s syndrome (pSS) patients. We report that EDA-A2 and its receptor XEDAR are overexpressed in pSS SGEC in comparison with healthy individuals and that the EDA-A2/XEDAR system in these cells is involved in the induction of apoptosis via caspases activation. Collectively, our results suggest that EDA-A2/XEDAR system may be a promising agent for the gene therapy of pSS.

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Titel: X-linked ectodermal dysplasia receptor (XEDAR) gene silencing prevents caspase-3-mediated apoptosis in Sjögren’s syndrome
verfasst von: Margherita Sisto
Loredana Lorusso
Sabrina Lisi
Publikationsdatum: 11.12.2015
Verlag: Springer International Publishing
Erschienen in: Clinical and Experimental Medicine / Ausgabe 1/2017
Print ISSN: 1591-8890
Elektronische ISSN: 1591-9528
DOI: https://doi.org/10.1007/s10238-015-0404-z

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X-linked ectodermal dysplasia receptor (XEDAR) gene silencing prevents caspase-3-mediated apoptosis in Sjögren’s syndrome

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