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Updated: Apr 21, 2026

Accelerated Type 1 Diabetes Induction in Mice by Adoptive Transfer of Diabetogenic CD4+ T Cells
Published on: May 6, 2013
Interleukin 2 in the pathogenesis and therapy of type 1 diabetes
Michelle Rosenzwajg1, Guillaume Churlaud, Agnès Hartemann
1Biotherapy (CIC-BTi) and Inflammation-Immunopathology-Biotherapy Department (i2B), AP-HP, Hôpital Pitié-Salpêtrière, 83 Boulevard de l'Hôpital, 75651, Paris, France, michelle.rosenzwajg@upmc.fr.
Abstract:
Regulatory T cells (Tregs) play a major role in controlling effector T cells (Teffs) responding to self-antigens, which cause autoimmune diseases. An improper Treg/Teff balance contributes to most autoimmune diseases, including type 1 diabetes (T1D). To restore a proper balance, blocking Teffs with immunosuppressants has been the only option, which was partly effective and too toxic. It now appears that expanding/activating Tregs with low-dose interleukin-2 (IL-2) could provide immunoregulation without immunosuppression. This is particularly interesting in T1D as Tregs from T1D patients are reported as dysfunctional and a relative deficiency in IL-2 production and/or IL-2-mediated signaling could contribute to this phenotype. A clinical study of low-dose IL-2 showed a very good safety profile and good Treg expansion/activation in T1D patients. This opens the way for efficacy trials to test low-dose IL-2 in prevention and treatment of T1D and to establish in which condition restoration of a proper Treg/Teff balance would be beneficial in the field of autoimmune and inflammatory diseases.
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