Interleukin 17 acts in synergy with B cell–activating factor to influence B cell biology and the pathophysiology of systemic lupus erythematosus

A Retraction to this article was published on 19 August 2014

This article has been updated

Abstract

Studies have suggested involvement of interleukin 17 (IL-17) in autoimmune diseases, although its effect on B cell biology has not been clearly established. Here we demonstrate that IL-17 alone or in combination with B cell–activating factor controlled the survival and proliferation of human B cells and their differentiation into immunoglobulin-secreting cells. This effect was mediated mainly through the nuclear factor-κB-regulated transcription factor Twist-1. In support of the relevance of our observations and the potential involvement of IL-17 in B cell biology, we found that the serum of patients with systemic lupus erythematosus had higher concentrations of IL-17 than did the serum of healthy people and that IL-17 abundance correlated with the disease severity of systemic lupus erythematosus.

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Figure 1: IL-17 and BAFF promote B cell survival in an NF-κB-dependent way.
Figure 2: Twist-1 mediates the antiapoptotic effects of IL-17 and BAFF through the induction of Twist-2 and Bfl-1.
Figure 3: IL-17 and BAFF promote the proliferation of B cells and their differentiation into immunoglobulin-secreting cells.
Figure 4: Effects of differentiation on the expression of TWIST1, TWIST2 and BCL2A1 in B cells.
Figure 5: Serum from patients with SLE induces the survival of peripheral B cells.
Figure 6: Serum from patients with SLE induces proliferation and differentiation into immunoglobulin-secreting cells.

Change history

  • 12 July 2013

    Despite many attempts to replicate these results, the authors have been unable to confirm the original data showing that IL-17 alone or in combination with B cell–activating factor controls the survival of human B cells (Fig. 1a,b). Because this weakens the conclusions of the paper, all the authors (except A.D. and P.T., who could not be contacted) now retract this paper.

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Acknowledgements

We thank H. Mitchison and G. Hinkal for critical reading of the manuscript; C. Delprat and G. Salles for scientific discussions; the laboratory of A. Puisieux (INSERM U590) for anti-Twist-1 as well as the Twist-1- and Twist-2-related vectors; and C. Bella for cell sorting. Supported by INSERM, UCB Lyon 1, the Arthritis Fondation Courtin (A.D.), the Association pour la Recherche sur le Cancer and the Ligue Contre le Cancer (07 and 26).

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N.B.-B. designed and supervised the study and wrote the manuscript; A.D. did all experiments presented in Figures 1,2,3,4,5,6 and Supplementary Figures 1,2,3,4,5,6; A.B. did statistical analysis and collected clinical data in Supplementary Tables 1 and 2; J.B. helped design the Twist-related experiments and wrote the manuscript; M.-C.T.-B. analyzed BCL2A1 expression in B cells from patients with SLE and healthy volunteers; B. Riche did statistical analysis; B. Ranchin, N.F., P.C., C.P.-N., P.T., I.D, J.T. and B.K. recruited patients; and S.A., A.P. and J.-F.E. contributed to the design and interpretation of experiments and to the editing of the manuscript.

Corresponding author

Correspondence to Nathalie Bonnefoy-Bérard.

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Supplementary Figures 1–6, Tables 1–2 and Supplementary Methods (PDF 2734 kb)

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Doreau, A., Belot, A., Bastid, J. et al. Interleukin 17 acts in synergy with B cell–activating factor to influence B cell biology and the pathophysiology of systemic lupus erythematosus. Nat Immunol 10, 778–785 (2009). https://doi.org/10.1038/ni.1741

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