Growth hormone prevents the development of autoimmune diabetes

Proc Natl Acad Sci U S A. 2013 Nov 26;110(48):E4619-27. doi: 10.1073/pnas.1314985110. Epub 2013 Nov 11.


Evidence supports a relationship between the neuroendocrine and the immune systems. Data from mice that overexpress or are deficient in growth hormone (GH) indicate that GH stimulates T and B-cell proliferation and Ig synthesis, and enhances maturation of myeloid progenitor cells. The effect of GH on autoimmune pathologies has nonetheless been little studied. Using a murine model of type 1 diabetes, a T-cell-mediated autoimmune disease characterized by immune cell infiltration of pancreatic islets and destruction of insulin-producing β-cells, we observed that sustained GH expression reduced prodromal disease symptoms and eliminated progression to overt diabetes. The effect involves several GH-mediated mechanisms; GH altered the cytokine environment, triggered anti-inflammatory macrophage (M2) polarization, maintained activity of the suppressor T-cell population, and limited Th17 cell plasticity. In addition, GH reduced apoptosis and/or increased the proliferative rate of β-cells. These results support a role for GH in immune response regulation and identify a unique target for therapeutic intervention in type 1 diabetes.

Keywords: Tregs; beta cells.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adoptive Transfer
  • Animals
  • Cytokines / blood
  • Diabetes Mellitus, Type 1 / prevention & control*
  • Flow Cytometry
  • Growth Hormone / pharmacology*
  • Immunohistochemistry
  • Insulin-Secreting Cells / physiology
  • Macrophages / drug effects
  • Macrophages / physiology
  • Mice
  • Mice, Transgenic
  • Prodromal Symptoms
  • Real-Time Polymerase Chain Reaction


  • Cytokines
  • Growth Hormone