It’s known that genetics, or an inherited genome, is a major determinant of one’s risk for autoimmune diseases, like Type 1 diabetes. In human cells, a person’s genome—about six feet of DNA—is compressed into the micrometer space of the nucleus via a three-dimensional folding process. Specialized proteins decode the genetic information, reading instruction from our genome in a sequence-specific manner. But what happens when a sequence variation leads to the misinterpretation of instruction, causing pathogenic misfolding of DNA inside the nucleus? Can the different folding patterns make us more susceptible to autoimmune diseases?
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