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

  • Sebastian Dolff1Email author,

    Affiliated with

    • Wayel H Abdulahad2 and

      Affiliated with

      • Cees GM Kallenberg2

        Affiliated with

        Arthritis Research & Therapy201416:409

        DOI: 10.1186/ar4576

        Published: 9 June 2014

        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.

        Declarations

        Authors’ Affiliations

        (1)
        Department of Nephrology, University Hospital Essen, University Duisburg-Essen
        (2)
        Department of Rheumatology and Clinical Immunology, University Medical Center Groningen, University of Groningen

        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.PubMedView Article
        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.View Article
        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 CentralPubMedView Article
        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.PubMedView Article

        Copyright

        © The Author(s) 2014

        This article is published under license to 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.

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