Promoting Immune Regulation in Type 1 Diabetes Using Low-Dose Interleukin-2

Connor J. Dwyer, Natasha C. Ward, Alberto Pugliese, Thomas R. Malek

Research output: Contribution to journalReview articlepeer-review

40 Scopus citations


Dysregulation of the immune system contributes to the breakdown of immune regulation, leading to autoimmune diseases, such as type 1 diabetes (T1D). Current therapies for T1D include daily insulin, due to pancreatic β-cell destruction to maintain blood glucose levels, suppressive immunotherapy to decrease the symptoms associated with autoimmunity, and islet transplantation. Genetic risks for T1D have been linked to IL-2 and IL-2R signaling pathways that lead to the breakdown of self-tolerance mechanisms, primarily through altered regulatory T cell (Treg) function and homeostasis. In attempt to correct such deficits, therapeutic administration of IL-2 at low doses has gained attention due to the capacity to boost Tregs without the unwanted stimulation of effector T cells. Preclinical and clinical studies utilizing low-dose IL-2 have shown promising results to expand Tregs due to their high selective sensitivity to respond to IL-2. These results suggest that low-dose IL-2 therapy represents a new class of immunotherapy for T1D by promoting immune regulation rather than broadly suppressing unwanted and beneficial immune responses.

Original languageEnglish (US)
Article number46
JournalCurrent diabetes reports
Issue number6
StatePublished - Jun 1 2016


  • IL-2
  • IL-2 receptor
  • Low-dose IL-2 therapy
  • Tolerance
  • Tregs
  • Type 1 diabetes

ASJC Scopus subject areas

  • Internal Medicine
  • Endocrinology, Diabetes and Metabolism


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