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Rapid induction of clinical remission by low-dose interleukin-2 in a patient with refractory SLE
  1. Jens Y Humrich1,
  2. Caroline von Spee-Mayer1,
  3. Elise Siegert1,
  4. Tobias Alexander1,
  5. Falk Hiepe1,
  6. Andreas Radbruch2,
  7. Gerd-Rüdiger Burmester1,
  8. Gabriela Riemekasten1
  1. 1Department of Rheumatology and Clinical Immunology, Charité—University Medicine Berlin, Berlin, Germany
  2. 2German Rheumatism Research Center (DRFZ), a Leibniz Institute, Berlin, Germany
  1. Correspondence to Dr Jens Y Humrich, Department of Rheumatology and Clinical Immunology, Charité—University Medicine Berlin, Charitéplatz 1, Berlin 10117, Germany; jens.humrich{at}charite.de

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Interleukin-2 (IL-2) is crucial for the growth and survival of regulatory T cells (Treg) and, thus, for the control of autoimmunity.1 ,2 In previous studies, we have proven a causal relationship between an acquired IL-2-deficiency, defects in Treg biology and the development of systemic lupus erythematosus (SLE).3 Accordingly, we showed that compensation of IL-2 deficiency by IL-2 therapy corrects associated Treg defects and ameliorates already established disease in lupus-prone mice.3 In line with this, two independent clinical studies showed recently that low-dose IL-2 induced expansion of the Treg pool and reduced clinical symptoms in two different immunological diseases without known IL-2 deficiency.4 ,5 These promising clinical findings in conjunction with preclinical data3 ,6 ,7 provide strong rationales for an IL-2-based immunotherapy of SLE in order to restore Treg activity and, thus, to re-establish endogenous mechanisms of tolerance that can counteract autoimmunity.

Here we report a rapid and robust reduction of disease activity in parallel with a remarkable expansion of the Treg population by low-dose IL-2 therapy in one patient with a long-term history of SLE and increased disease activity refractory …

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Footnotes

  • Funding This study was supported by grants from the Deutsche Forschungsgemeinschaft (SFB650, TP10) and the Charité—University Medicine Berlin.

  • Contributors Study concept and design: JYH, TA, FH, AR, G-RB, GR. Acquisition of data: JYH, CvS-M, ES. Analysis and interpretation of data: JYH, CvS-M, TA and GR. Drafting of the manuscript: JYH and GR. Study supervision: JYH and GR.

  • Competing interests None.

  • Ethics approval This study was announced as ‘off-label’ therapy to the institutional Ethics Committee of the Charité—University Medicine Berlin. Written informed consent was obtained from the patient prior to the initiation of the off-label treatment with aldesleukin according to the Declaration of Helsinki in the revised version of 1996, and the International Conference on Harmonization (ICH) guidelines on Good Clinical Practice (GCP).

  • Provenance and peer review Not commissioned; externally peer reviewed.

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