Copycat proteins may trigger type 1 diabetes
Despite the fact that it appears in childhood and has several genetic risk factors, autoimmune type 1 diabetes cannot be entirely predicted by genetics. Only one identical twin may get the disease, for instance. New research suggests how an environmental factor—gut bacteria—could play a role.
According to the study, led by Li Wen, M.D., Ph.D., senior research scientist in medicine (endocrinology), Fusobacteria in the guts of mice produce proteins that mimic the structure of molecules in insulin producing pancreatic beta cells, the same cells that are destroyed in type 1 diabetes.
As the number of Fusobacteria in mice increases, the immune system produces more T cells that recognize these molecules, spurring immune activity not only against the bacteria, but also against the pancreatic cells.
In mice with a genetic risk factor for type 1 diabetes, having excess Fusobacteria in their guts accelerated the onset of disease. Moreover, altering their guts to decrease Fusobacteria reversed the development of type 1 diabetes, the researchers reported Sept. 12 in Journal of Experimental Medicine.
The new findings could eventually provide targets for new therapies in humans with type 1 diabetes.