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Not a peripheral story

Beyond peripheral autoimmunity in Type I diabetes

By sourcing T cells directly from the pancreatic islets of Type I diabetes patients, rather than the standard method of taking blood samples, an academic team has provided an unprecedented view into the molecules that drive the autoimmune disease. The results indicate there are dozens, if not hundreds, of new antigens yet to be characterized, with each one providing another chance at invoking the long-sought strategy of antigen-specific tolerance.

Virtually all studies of the antigens fueling Type I diabetes in humans have come from investigating self-damaging T cells in blood samples. That raises the question of whether the full repertoire of the cells and the pancreatic antigens they recognize might be larger than what can be observed outside the organ.

Moreover, while therapies based on peripherally identified antigens, such as proinsulin and GAD, successfully treated mouse models of the disease, they subsequently failed in the clinic or were shelved prior to large efficacy trials, making it unclear whether those antigens play a major role in the diseased tissue.

In a Nature Medicine study published last month, a team led by Sally Kent, an associate professor of medicine at the University of Massachusetts Medical School, cloned 236 self-reactive T cell lines derived directly from pancreatic islets of nine patients, whose tissue was donated

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