Irene Marafini, Maria Grazia Imeneo and Giovanni Monteleone
Celiac disease (CD) is a chronic enteropathy that develops in genetically-predisposed individuals after the ingestion of gluten. The small intestinal damage observed in CD patients is characterized by villous atrophy, crypt hyperplasia and massive infiltration of the mucosa with inflammatory cells. The molecular mechanisms that trigger and amplify inflammatory signals in CD are not fully understood. There is evidence that excessive activation of some subsets of Natural Killer (NK) cells occurs in CD and can contribute to the perpetuation of gluten-driven immune response and intestinal damage. On the other hand, the active phases of the disease are also marked by reduced mucosal presence of a specific subpopulation of NK cells expressing activating receptors and producing IL-22, a cytokine involved in the maintenance of intestinal barrier and immune homeostasis. In this article, we shortly revise the current literature on the role of NK cells in CD.