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Abstract Number: 2737

Microrna-155 Suppresses IL-21 Signaling and Production in Systemic Lupus Erythematosus

Tue K. Rasmussen1, Thomas Andersen1, Rasmus Bak1, Gloria Yiu2, Kristian Steengaard-Petersen3, Jacob G. Mikkelsen1, Paul J. Utz4, Christian Holm1 and Bent Deleuran3,5, 1Department of Biomedicine, Aarhus University, Aarhus C, Denmark, 2Department of Medicine, Division of Immunology and Rheumatology, Stanford University School of Medicine, Stanford, CA, 3Department of Rheumatology, Aarhus University Hospital, Aarhus, Denmark, 4Medicine, Stanford University School of Medicine, Stanford, CA, 5Department of Biomedicine, Aarhus University, Aarhus, Denmark

Meeting: 2014 ACR/ARHP Annual Meeting

Keywords: Cell Signaling, MicroRNA, SLE, T cells and interleukins (IL)

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Session Information

Session Title: T cell Biology in Lupus, Vasculitis, Myositis and Other Autoimmunity

Session Type: Abstract Submissions (ACR)

Background/Purpose

IL-21 is a key regulator of B cells functions and autoantibody production and is mainly produced by follicular T helper cells. The purpose of this study is to investigate the signaling capacity of interleukin (IL)-21 in T and B cells and assess its possible regulation by microRNA-155 and its target gene suppressor of cytokine signaling 1 (SOCS1) in systemic lupus erythematosus (SLE). 

Methods

The signaling capacity of IL-21 was quantified by stimulating PBMCs with IL-21 and measuring phosphorylation of (p)STAT3 in CD4+ T cells, B cells, and NK cells. Induction of miR-155 by IL-21 was investigated by stimulating purified CD4+ T cells with IL-21 and measuring miR-155 expression levels. The functional role of miR-155 was assessed by overexpressing miR-155 in PBMCs from SLE patients and HCs and measuring its effects on STAT3 and IL-21 production in CD4+ and CD8+ T cells. 

Results

Induction of pSTAT3 in CD4+ T cells in response to IL-21 was significantly decreased in SLE patients compared to HCs (p<0.0001). Further, expression levels of miR-155 were significantly decreased and SOCS1 correspondingly increased in CD4+ T cells from SLE patients. Finally, overexpression of miR-155 in CD4+ T cells increased STAT3 phosphorylation in response to IL-21 treatment (p<0.01) and differentially increased IL-21 production in SLE patients compared to HCs (p<0.01).

Conclusion

We demonstrate that SLE patients have reduced IL-21 signaling capacity, decreased miR-155 levels, and increased SOCS1 levels compared to HCs. The reduced IL-21 signaling in SLE could be rescued by overexpression of miR-155, suggesting an important role for miR-155 in the reduced IL-21 signaling observed in SLE.


Disclosure:

T. K. Rasmussen,
None;

T. Andersen,
None;

R. Bak,
None;

G. Yiu,
None;

K. Steengaard-Petersen,
None;

J. G. Mikkelsen,
None;

P. J. Utz,
None;

C. Holm,
None;

B. Deleuran,
None.

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