Abstract
Type 1 diabetes (T1D) is an autoimmune disease that affects approximately 34 million people around the world. T1D is caused by the destruction of insulin-producing pancreatic β-cells by autoreactive T cells that lack effective immune regulation. One of the most common animal models for diabetes study is the NOD (non-obese diabetic) mouse strain. Using female NOD mice, which develop spontaneous T1D, we observed that growth hormone (GH) induces a protective effect on insulin-producing cells and as a result, inhibits T1D development. We generated a transgenic NOD mouse that expresses bovine GH and showed almost complete protection against diabetes development. Histochemical analysis demonstrated an increase in the number of pancreatic endocrine progenitor cells, overgrowth of islets of Langerhans, and although these mice showed peri-insulitis, infiltration was much reduced. The mechanism involved an increase in regulatory T cell number and activity, a polarization phenotype toward anti-inflammatory macrophages, and altered B cell responses with reduced antibody production. Our results identify a regulatory role for GH in immune cells and pinpoint a new target for therapeutic intervention on type 1 diabetes.
- Copyright © 2013 by The American Association of Immunologists, Inc.
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