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Open Access Letter

Response to ‘T-helper 17 cell cytokines and interferon type I: partners in crime in systemic lupus erythematosus?’

Sebastian Dolff1*, Wayel H Abdulahad2 and Cees GM Kallenberg2

Author Affiliations

1 Department of Nephrology, University Hospital Essen, University Duisburg-Essen, Hufelandstr. 55, 45122 Essen, Germany

2 Department of Rheumatology and Clinical Immunology, University Medical Center Groningen, University of Groningen, Hanzeplain 1, 9713 GZ, Groningen, The Netherlands

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Arthritis Research & Therapy 2014, 16:409  doi:10.1186/ar4576


See related research by Brkic et al., http://arthritis-research.com/content/16/2/R62 and related letter by Brkic et al., http://arthritis-research.com/content/16/3/410


The electronic version of this article is the complete one and can be found online at: http://arthritis-research.com/content/16/3/409


Published:9 June 2014

© 2014 Dolff et al.; licensee BioMed Central Ltd.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

Letter

We read with great interest the article by Brkic and colleagues in a recent issue of Arthritis Research & Therapy[1]. In that study, the authors investigated the distribution of T helper (Th) subsets which produce IL-17A, IL-17 F, IL-21, and IL-22 in patients with systemic lupus erythematosus (SLE) in relation to their genetic IFN type I signature. Patients with an IFN type I-positive signature showed increased percentages of IL-17A- and IL-21-producing CCR6+ T cells. From these results, the authors conclude that IFN type I cells co-act with Th17 cytokines in the pathogenesis of SLE. Surprisingly, they excluded CD25+ T cells from their analysis. In a previous study, we showed that Th cells from SLE patients expressing CD25med and CD25high are also able to produce IFN-γ and IL-17A [2]. Therefore, it would be relevant to assess cytokine expression in CD4+CD25+ T cells from IFN type I-positive and IFN type I-negative SLE patients. Furthermore, it should be proven that the genetic signature is solely responsible for the increased IFN production by Th cells. In addition, their finding that CCR6+ T cells are capable of producing IL-21 indirectly confirms our previous observation that IL-17+ T cells are a main source of IL-21 in patients with SLE [3]. Possibly, IL-21 is orchestrating the Th1/Th17 axis.

Finally, we agree that there might be a co-activity between IFN-I- and IL-17-producing cells as described by Brkic and colleagues. However, considering our findings that T cells with a regulatory phenotype are able to produce IFN-γ and IL-17A in patients with SLE, we suggest that primarily the plasticity of T cells is altered in patients with SLE [4].

Abbreviations

IFN: Interferon; IL: Interleukin; SLE: Systemic lupus erythematosus; Th: T helper.

Competing interests

The authors declare that they have no competing interests.

Authors’ contributions

All authors contributed to the interpretation of data. SD drafted the manuscript. All authors read and approved the final manuscript.

References

  1. Brkic Z, Corneth OB, van Helden-Meeuwsen CG, Dolhain RJ, Maria NI, Paulissen SM, Davelaar N, van Hamburg JP, van Daele PL, Dalm VA, van Hagen PM, Hazes JM, Versnel MA, Lubberts E: T-helper 17 cell cytokines and interferon type I: partners in crime in systemic lupus erythematosus?

    Arthritis Res Ther 2014, 16:R62. PubMed Abstract | BioMed Central Full Text OpenURL

  2. Dolff S, Bijl M, Huitema MG, Limburg PC, Kallenberg CG, Abdulahad WH: Disturbed Th1, Th2, Th17 and Treg balance in patients with systemic lupus erythematosus.

    Clin Immunol 2011, 141:120-197. OpenURL

  3. Dolff S, Abdulahad WH, Westra J, Doornbos-van Der Meer B, Limburg PC, Kallenberg CG, Bijl M: Increase in IL-21 producing T-cells in patients with systemic lupus erythematosus (SLE).

    Arthritis Res Ther 2011, 13:R157. PubMed Abstract | BioMed Central Full Text | PubMed Central Full Text OpenURL

  4. Koenen HJ, Smeets RL, Vink PM, van Rijssen E, Boots AM, Joosten I: Human CD25highFoxp3pos regulatory T cells differentiate into IL-17-producing cells.

    Blood 2008, 112:2340-2352. PubMed Abstract | Publisher Full Text OpenURL