Interleukin-2 (IL-2) is crucial for the growth and survival of regulatory T cells (Treg), and thus for the control of autoimmunity. In previous studies we have proven the significance of an acquired IL-2 deficiency and related Treg defects in the pathogenesis of systemic lupus erythematosus (SLE). 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 (1). Proceeding to a clinical translation, we recently reported a rapid and robust reduction of disease activity in parallel to a remarkable expansion of the Treg population by low-dose IL-2 therapy in one patient with refractory SLE (2). Together, these studies provided the rationales for the clinical implementation an IL-2-based immunotherapy for the treatment of SLE with the aim to restore Treg activity and thus to re-establish endogenous mechanisms of immune tolerance.
Here, first promising results from the ongoing phase I/IIa clinical trial (PRO-IMMUN) addressing the safety, tolerability, immunological responses and clinical efficacy of a subcutaneous low-dose IL-2 therapy in patients with refractory SLE will be presented.
Humrich JY, et al. (2010) Homeostatic imbalance of regulatory and effector T cells due to IL-2 deprivation amplifies murine lupus. Proc Natl Acad Sci USA 107(1):204-209.
Humrich JY, et al. (2015) Rapid induction of clinical remission by low-dose interleukin-2 in a patient with refractory SLE. Ann Rheum Dis. doi: 10.1136/annrheumdis-2014-206506.
Disclosure of Interest None declared