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. 2018 Mar 1:2018:6103064.
doi: 10.1155/2018/6103064. eCollection 2018.

Soluble Interleukin-2 Receptor: A Potential Marker for Monitoring Disease Activity in IgG4-Related Disease

A F Karim  1 , L E M Eurelings  1 , R D Bansie  1 , P M van Hagen  1   2 , J A M van Laar  1   2 , W A Dik  3
Affiliations

Soluble Interleukin-2 Receptor: A Potential Marker for Monitoring Disease Activity in IgG4-Related Disease

A F Karim et al. Mediators Inflamm. .

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.

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Figures

Figure 1
Figure 1
Boxplot of serum sIL-2R levels. Boxplots of serum sIL-2R (pg/ml) in newly untreated sarcoidosis and IgG4-RD and sIL-2R levels after initiation of treatment in IgG4-RD and in control population. ∗P = 0.004; ∗∗P < 0.001; ∗∗∗P = 0.001.
Figure 2
Figure 2
Correlation between sIL-2R and IgG4-RD RI. Correlation between sIL-2R and IgG4-RD RI before and after treatment (a) and correlation between the decrease in IgG4-RD RI after treatment and the decrease in sIL-2R levels after treatment (b).
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References

    1. Karim A. F., Verdijk R. M., Guenoun J., van Hagen P., van Laar J. An inflammatory condition with different faces: immunoglobulin G4-related disease. The Netherlands Journal of Medicine. 2016;74(3):110–115. - PubMed
    1. Kamisawa T., Zen Y., Pillai S., Stone J. H. IgG4-related disease. The Lancet. 2014;385(9976):1460–1471. doi: 10.1016/S0140-6736(14)60720-0. - DOI - PubMed
    1. Karim F., de Hoog J., Paridaens D., et al. IgG4-related disease as an emerging cause of scleritis. Acta Ophthalmologica. 2017;95(8):e795–e796. doi: 10.1111/aos.13376. - DOI - PubMed
    1. Karim F., Loeffen J., Bramer W., et al. IgG4-related disease: a systematic review of this unrecognized disease in pediatrics. Pediatric Rheumatology. 2016;14(1):p. 18. doi: 10.1186/s12969-016-0079-3. - DOI - PMC - PubMed
    1. Karim F., Groningen M. C.-v., van Laar J. A. M. AA amyloidosis and IgG4-related disease. The New England Journal of Medicine. 2017;376(6):599–600. doi: 10.1056/NEJMc1614275. - DOI - PubMed

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