Article Text

SP0189 Induction of Remission by Low-Dose IL-2-Therapy in One SLE Patient with Increased Disease Activity Refractory to Standard Therapies
  1. J.Y. Humrich
  1. Rheumatology and Clinical Immunology, Charité - Universitätsmedizin Berlin, Berlin, Germany


IL-2 deficiency and associated regulatory T cell (Treg) defects critically contribute to SLE pathogenesis. In our previous translational work we proved the efficacy and safety of a low-dose IL-2 therapy in animal models and identified a reversible IL-2 deprivation of Treg also in human SLE patients. Together, these studies provided the 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 that a cyclic and subcutaneously applied low-dose IL-2-therapy induced a rapid, strong and sustained reduction of disease activity in parallel to a remarkable and selective expansion of the Treg population in a SLE patient with increased disease activity (SELENA-SLEDAI 14) refractory to a large variety of approved and experimental therapies. Already after the first therapeutic cycle, signs of arthritis and later also myositis and active skin eruptions disappeared. In addition, levels of anti-dsDNA antibodies dramatically declined (ELISA) or even turned negative (Crithidia IFT). Throughout the residual three therapeutic cycles, organ manifestations remained absent and disease activity remained low with a SELENA-SLEDAI of 4. In addition, the daily dose of glucocorticosteroids could be reduced from 30 mg/d at baseline to 10 mg/d after the 4th and last therapeutic cycle. The therapy was very well tolerated and adverse events were minimal suggesting that this therapy is very safe in SLE patients.

In summary, these data provide the first evidence for the clinical efficacy and safety of a subcutaneous low-dose IL-2-therapy in conjunction with the in vivo augmentation of Treg activity in SLE patients and strongly support the rationales of this biologic and patho-physiologically-driven therapeutic approach.

Disclosure of Interest None declared

DOI 10.1136/annrheumdis-2014-eular.6341

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