Two recent reports offer a taste to the little-known underlying immunological mechanisms of celiac disease, a digestive autoimmune disorder triggered by gluten protein, which affects as many as 1 in 100 people in the United States.
Working ex vivo, a University of Chicago group found that interleukin-15 overexpression helps convert antigen-specific cytotoxic T lymphocytes (CTLs) into rogue lymphokine-activated killers (LAKs) via the CTL receptor NKG2D.1 The LAK cells provoke a more general immune response that destroys the intestinal lining and results in poor nutrient absorption, the root cause of the disease's myriad complications (which range from diarrhea to lymphoma).
In another paper, a group at Equipe Avenir-INSERM in Paris reports that epithelial cells in the intestine are targeted for destruction due to high levels of a molecule called MICA, which is recognized the NKG2D receptor.2 Researchers still don't understand, however, why gluten induces IL-15 or MICA in some persons and ...
