Researchers at National Jewish Health and the University of Colorado Anschutz Medical Campus have identified the precise protein fragment, or peptide, that can trigger diabetes in mice. The finding, published in the June 15, 2010, issue of the Proceedings of the National Academy of Sciences, supports an emerging theory about the origins of autoimmunity, and may lead to new diagnostic and therapeutic strategies in humans.
“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.”
The immune system tries to delete all T cells that might cause autoimmune disease. During development in the thymus, immature T cells are exposed to “self” protein fragments, which are part of the organism. T cells that recognize and bind to them are destroyed. This process, however, is not foolproof, and autoimmune T cells do occasionally escape.