Abstract
Nonobese diabetic (NOD) mice spontaneously develop autoimmune diabetes, bearing close resemblance to the human condition. The disease is mediated by auto-specific T cells, which infiltrate the pancreatic islets and destroy insulin-producing β cells. A hallmark of the disease is the de novo generation of lymph-node-like structures in the pancreas, which are essential for progression of the disease. A large body of evidence implicates lymphotoxin (LT) in the formation of these lymphoid structures and the production of follicular dendritic cells. In support of this notion, the ectopic expression of LT can result in the in situ generation of lymph-node-like organs in the periphery. Hence, it was supposed that the formation of organized lymphoid structures in the pancreas of NOD mice might be regulated by LT.
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