Prion disorders riddle the mammalian brain with plaque and holes, the precise pattern and resulting symptoms--dementia, extreme fatigue, or loss of balance--depending on whether one is human, bovine, or ovine. The agent of such a transmissible spongiform encephalopathy (TSE) is an infectious form of prion protein, called PrP scrapie (PrPSc), named after the long-known sheep illness. In bovine spongiform encephalopathy (mad cow disease) and its human version, variant Creutzfeldt-Jakob disease (vCJD), ingested PrPSc converts the normal "cellular" form of PrP (PrPC) to an abnormal form.

Until now, most prion research explored brain tissue--the end point of infection. But a few investigators are seeking the site where prions pathogenesis begins. And their work is converging on a little-mentioned resident of the intestinal lining called an M cell.

M cells link the digestive and immune systems.1 They provide a portal for ingested bacteria and viruses to lymphoid tissue beneath the intestinal...

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