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|Title:||ARA3 Inflammasome activation in salivary gland epithelial cells - a disease model for primary sjögren's syndrome|
|Other Titles:||ARA3 Inflammasome activation in salivary gland epithelial cells - a disease model for primary sjogren's syndrome|
|Citation:||Abstracts of the Australian Rheumatology Associationin conjunction with Rheumatology Health Professionals Association, 56th Annual Scientific Meeting, as published in Internal Medicine Journal, 2015 / vol.45, iss.Suppl. 2, pp.1|
|Conference Name:||Australian Rheumatology Associationin conjunction with Rheumatology Health Professionals Association, 56th Annual Scientific Meeting (23 May 2015 - 26 May 2015 : Adelaide, South Australia)|
|Lau A, Bosco M, Lester S, Roscioli E, Zalewski P, Rischmueller M|
|Abstract:||AIM: Primary Sjögren’s Syndrome (pSS) is an autoimmune inﬂammatorydisease affecting salivary glandular epithelium. It is characterised by thepresence of immune complexes comprising autoantibodies bound to RNA/protein, which correlate with disease severity and potentially drive inﬂam-mation. Inﬂammasomes are a component of the innate immune systemthought to play a role in immune surveillance of mucosal surfaces. Wehypothesise that inﬂammasome activation by immune complexes may playa key role in salivary gland inﬂammation in pSS. In immune cells, inﬂammasomeactivation requires both priming through toll-like receptors (eg LPS-TLR4for NLRP3), followed by speciﬁc activation. However, nothing is knownabout inﬂammasome priming in salivary gland epithelial cells (SGEC).The aim of this study was to examine TLR priming, of both NLRP3 andAIM2 inﬂammasomes in a human, secondary SGEC line.METHODS: A253 cells were primed with PolyIC (TLR 3), LPS (TLR4),Imiquimod (TLR 7) and CL264 (TLR 7) for 6 hours. Changes in transcript/protein levels were measured by both qPCR, western blotting and immu-nocytochemistry.RESULTS: NLRP3 was lowly expressed, by both qPCR and western blot, andwas not induced by any TLR ligands. However, polyIC upregulated bothAIM2 and IL-1beta as shown by both qPCR (6-fold and 3-fold respectively,p < 0.05) and western blot. Preliminary immunohistochemistry demon-strates AIM2 staining of the epithelium lining the ducts and acini of salivarygland biopsies from both pSS patients and controls.CONCLUSIONS: The AIM2 inﬂammasome is expressed in SGEC lining theducts and acini, and polyIC, a dsRNA analogue, primes the AIM2inﬂammasome in the A253 SGEC cell line. These results support a poten-tial role for inﬂammasome activation in SGEC in pSS, possibly mediated byRNA containing immune complexes which are present in this disease. TheA253 SGEC cell line may be a suitable model to further investigateinﬂammasome activation by immune complexes in epithelial cells.|
|Rights:||© 2015 The Authors|
|Appears in Collections:||Medicine publications|
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