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Growth hormone prevents the development of autoimmune diabetes

Villares, Ricardo, Kakabadse, Dimitri, Juarranz, Yasmina, Gomariz, Rosa P., Martínez-A, Carlos, Mellado, Mario
Proceedings of the National Academy of Sciences of the United States of America 2013 v.110 no.48 pp. E4619
B-lymphocytes, T-lymphocytes, animal models, apoptosis, autoimmune diseases, cytokines, immune response, insulin-dependent diabetes mellitus, islets of Langerhans, macrophages, mice, somatotropin, stem cells
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.