Session Title: Sjögren's Syndrome - Poster I: Translational Science
Session Type: ACR Poster Session A
Session Time: 9:00AM-11:00AM
Background/Purpose: Type-III IFNs or IFNλs(IFNλ1/IL29, IFNλ2/IL28A and IFNλ3/IL28B) consist a recently identified group of IFNs,initiallyimplicated inseveral human diseases, including cancer and autoimmunity. In this study, we sought to investigatethe expression of type-III IFNs (IFNλ1/IL29, IFNλ2/IL28A and IFNλ3/IL28B) and their common receptor IFNλR1/IL28Ra in Sjögren’s Syndrome (SS).
Methods: The in situ expression of all molecules was studied immunohistochemically in minor salivary gland tissues (MSG) from primary SS-patients (n=46) and sicca-complaining controls (n=17). Expression in peripheral blood mononuclear cells (PBMCs) and sera was investigated by ELISA and real-time PCR, respectively. Expression in resting or TLR-stimulated salivary gland epithelial cells (SGEC) was assessed by both qPCR and ELISA.
Results: All type-III IFN family members were detected in ductal and acinar epithelia of MSGs from both SS-patients and sicca-controls.IFNλ2/IL28A and IFNλ3/IL28B were also expressed in infiltrating mononuclear cells (MNCs). In SS-patients with intermediate MSG lesions, the epithelial expression of IFNλ2/IL28A was more intense (p<0.05) compared to sicca-controls. The receptor IFNλR1/IL28Ra was detected in all types of cells except fibroblasts and was exceptionally strong in plasmatocytoid dendritic-cells, indicating that they are susceptible to type-III IFN-mediated regulation.Although none of the type-III IFNs was constitutively expressed in SGECs, they were all readily induced by TLR3 stimulation, suggesting that the in situepithelial expression can be attributed to local microenvironment. Type-III IFN-mRNAs were not expressed in PBMCs, whereas only IFNλ1/IL29 was detected in the sera and was significantly elevated in SS patients with intermediate MSG inflammatory lesions compared to sicca-controls (p<0.0053).
Conclusion: Type-III IFNs are expressed in the MSGs and their expression is likely subjected to micro-environmental regulation. Our findings suggest that they may be implicated in SS pathogenesis.
To cite this abstract in AMA style:Apostolou E, Kapsogeorgou EK, Konsta OD, Giotakis I, Saridaki MI, Andreakos E, Tzioufas AG. Expression of Type-III Interferons (IFNλs) and Their Receptor in Sjögren’s Syndrome [abstract]. Arthritis Rheumatol. 2016; 68 (suppl 10). https://acrabstracts.org/abstract/expression-of-type-iii-interferons-ifn%ce%bbs-and-their-receptor-in-sjogrens-syndrome/. Accessed December 3, 2020.
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