![]() ![]() Taken together, our data reveal previously unknown activities as well as suggest that the ligand for the sIL-13R might be a component of the IL-13R complex or a counterstructure yet to be defined. We thus propose that IL-13R alpha 1 is a molecule involved in B cell differentiation, using a mechanism that may involve regulation of IL-6-responsive elements. When sIL-13R was injected into mice, it served as an adjuvant-promoting production to varying degrees of IgM and IgG isotypes. ![]() Furthermore, the effects of the sIL-13R molecule were inhibited in the presence of an anti-IL-13 mAb, and preincubation of GC cells with IL-13 enhanced the sIL-13R-mediated effects. In GC cell cultures, sIL-13R also promoted IL-6 production, and interestingly, sIL-13R-induced IgG 2 a and IgG 2 b augmentation was absent in GC cells isolated from IL-6-deficient mice. These effects were enhanced by CD40 signaling and were not inhibited by an anti-IL4R alpha mAb, a result suggesting other ligands. The sIL-13R promotes proliferation and augmentation of Ag-specific IgM, IgG 2 a, and IgG 2 b production by murine germinal center (GC) B cells in vitro. Using a soluble form of the murine IL-13R alpha 1 (sIL-13R), we reveal several novel features of this system. Poudrier, J Graber, P Herren, S Gretener, D Elson, G Berney, C Gauchat, J F Kosco-Vilbois, M HĪ functional IL-13R involves at least two cell surface proteins, the IL-13R alpha 1 and IL-4R alpha. No commercial use is permitted unless otherwise expressly granted.Ī soluble form of IL-13 receptor alpha 1 promotes IgG 2 a and IgG 2 b production by murine germinal center B cells. © Article author(s) (or their employer(s) unless otherwise stated in the text of the article) 2017. Tissue IgG 2 and IgG4 subclass reporting may provide additional insight regarding the ' IgG4-RD' pathogenesis. A serum IgG 2 cut-off >5.3 g/L was found to be 80% sensitive and 91.7% specific for orbital IgG4-RD, with an accuracy of 0.90. Significant elevations of serum IgG 2 and tissue IgG 2 plasma cells are present in orbital IgG4-RD in comparison with non-IgG4 orbital inflammation (idiopathic and autoimmune OID), suggesting that IgG 2 may play a role in IgG4-RD. Similarly, significant elevation of tissue IgG 2 plasma cells was also seen among IgG4-RD (group 1), idiopathic and autoimmune OID (groups 2 and 3). Significant (twofold) serum IgG 2 elevation was noted among IgG4-RD (group 1), idiopathic (group 2) and autoimmune OID (group 3). Dual IHC showed IgG 2 plasma cells as a distinct population from IgG4 plasma cells. Serum IgG 1, IgG 2, IgG3 and IgG4 levels were collated where available and immunohistochemistry (IHC) for tissue IgG 2 plasma cells was performed. Clinical information and histology were reviewed and cases were classified into three groups: Group 1: IgG4-RD orbital inflammation (n=43) Group 2: idiopathic OID (n=12) and Group 3: autoimmune OID (n=14). This is an international (Sheffield, UK, and Singapore) collaborative, retrospective case review of 69 patients (38 from Singapore National Eye Centre and 31 from Royal Hallamshire Hospital, Sheffield) with orbital inflammatory biopsies between 20. To determine the role of serum and tissue IgG 2 in orbital biopsies with the histological features of IgG4-related disease ( IgG4-RD) in comparison with non-IgG4-related orbital inflammatory disorders (OID), including autoimmune disorders. Serum IgG 2 and tissue IgG 2 plasma cell elevation in orbital IgG4-related disease ( IgG4-RD): Potential use in IgG4-RD assessment.Ĭhan, Anita S Y Mudhar, Hardeep Shen, Sunny Yu Lang, Stephanie S Fernando, Malee Hilmy, Maryam Hazly Guppy, Naomi Jayne Rennie, Ian Dunkley, Lisa Al Jajeh, Issam ![]()
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