IL-2 reverses established type 1 diabetes in NOD mice by a local effect on pancreatic regulatory T cells

Yenkel Grinberg‐Bleyer(Inserm), Audrey Baeyens(Inserm), Sylvaine You(Hôpital Necker-Enfants Malades), Rima Elhage(Inserm), Gwladys Fourcade(Inserm), Sylvie Grégoire(Inserm), Nicolas Cagnard(Hôpital Necker-Enfants Malades), Wassila Carpentier(Sorbonne Université), Qizhi Tang(University of California, San Francisco), Jeffrey A. Bluestone(University of California, San Francisco), Lucienne Chatenoud(Hôpital Necker-Enfants Malades), David Klatzmann(Inserm), Benoı̂t L. Salomon(Inserm), Eliane Piaggio(Inserm)
The Journal of Experimental Medicine
August 2, 2010
Cited by 417Open Access
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Abstract

Regulatory T cells (T reg cells) play a major role in controlling the pathogenic autoimmune process in type 1 diabetes (T1D). Interleukin 2 (IL-2), a cytokine which promotes T reg cell survival and function, may thus have therapeutic efficacy in T1D. We show that 5 d of low-dose IL-2 administration starting at the time of T1D onset can reverse established disease in NOD (nonobese diabetic) mice, with long-lasting effects. Low-dose IL-2 increases the number of T reg cells in the pancreas and induces expression of T reg cell-associated proteins including Foxp3, CD25, CTLA-4, ICOS (inducible T cell costimulator), and GITR (glucocorticoid-induced TNF receptor) in these cells. Treatment also suppresses interferon gamma production by pancreas-infiltrating T cells. Transcriptome analyses show that low-dose IL-2 exerts much greater influence on gene expression of T reg cells than effector T cells (T eff cells), suggesting that nonspecific activation of pathogenic T eff cells is less likely. We provide the first preclinical data showing that low-dose IL-2 can reverse established T1D, suggesting that this treatment merits evaluation in patients with T1D.


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