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Author Karim, A. F. ♦ Eurelings, L. E. M. ♦ Bansie, R. D. ♦ van Hagen, P. M. ♦ van Laar, J. A. M. ♦ Dik, W. A.
Editor Giovarelli, Mirella
Source Hindawi
Content type Text
Publisher Hindawi
File Format PDF
Copyright Year ©2018
Language English
Abstract Background. IgG4-related disease (IgG4-RD) is a fibroinflammatory condition. T-cells play a crucial role in the pathogenesis, and therefore, serum soluble interleukin-2 receptor (sIL-2R) may be a potential biomarker. Method. We studied the levels of sIL-2R in 26 histologically proven IgG4-RD patients with available serum sIL-2R and compared them to those in newly diagnosed and untreated sarcoidosis patients (n=78) and controls (n=101) and the serum sIL-2R levels in patients after treatment of IgG4-RD (n=15). The disease activity was measured using the IgG4-Related Disease Responder Index (IgG4-RD RI). Results. Median serum sIL-2R in IgG4-RD patients was 4667 pg/ml compared to 1515 pg/ml in controls (P<0.001) and 6050 pg/ml in sarcoidosis patients (P=0.004 compared to IgG4-RD). All IgG4-RD patients had elevated serum sIL-2R levels compared to the reference value of <2500 pg/ml in controls and 85% elevated serum IgG4; however, these did not correlate with each other. Both serum sIL-2R and IgG4 levels declined significantly after treatment (P=0.001 and P=0.01, resp.). Before treatment, serum sIL-2R level and IgG4-RD RI did not correlate with each other. However, the decrease in serum sIL-2R upon treatment did correlate significantly (P=0.04) with the decrease in disease activity assessed by IgG-RD RI. Conclusion. Serum sIL-2R is elevated in IgG4-RD reflecting the inflammatory process with enhanced T-cell activation. Furthermore, serum sIL-2R might serve as a potential marker of response to treatment in IgG4-RD.
ISSN 09629351
Learning Resource Type Article
Publisher Date 2018-03-01
Rights License 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.
e-ISSN 14661861
Journal Mediators of Inflammation
Volume Number 2018
Page Count 6


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