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

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

Research output: Contribution to journalArticle

26 Scopus citations

Abstract

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
Volume16
Issue number6
DOIs
StatePublished - Jun 1 2016

Keywords

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

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Internal Medicine

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