Researchers say they have identified the protein fragment (peptide) that causes Type 1 diabetes in mice.
The findings challenge conventional thinking about the origins of Type 1 diabetes in humans, according to the researchers from National Jewish Health and the University of Colorado Anschutz Medical Campus. “Our findings contradict conventional wisdom, which suggests that insulin peptides that are well presented to the immune system trigger diabetes,” said John Kappler, PhD, Professor of Immunology at National Jewish Health. “We believe, however, that the peptide we identified triggers diabetes precisely because it is so poorly presented to the immune system.”
Type 1 diabetes is caused when rogue autoimmune cells attack insulin-producing cells in the pancreas, destroying them.
The researchers say that the immune system tries to delete all these rogue T-cells that might cause autoimmune disease. However, autoimmune T cells do occasionally escape. Findings from the most recent study support a theory recently posited by Kappler, Eisenbarth, and Brian Stadinski, PhD, of Harvard Medical School. They believe that poorly presented peptides are more likely to cause diabetes and other autoimmune diseases, because they allow autoimmune T cells to escape deletion. Once they begin circulating in the body, these T cells are stimulated when they encounter high concentrations of the peptide or peptides that have been processed differently.
Researchers hope the discovery ill lead to new treatments for diabetes.
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