The Role of Natural Killer Receptors in Celiac DiseaseIrene Marafini1, Maria Grazia Imeneo2 and Giovanni Monteleone1*
- *Corresponding Author:
- Giovanni Monteleone
Department of Systems Medicine, University of Rome Tor Vergata
Via Montpellier, 100133 Rome, Italy
E-mail: [email protected]
Received date: December 16, 2016; Accepted date: January 16, 2017; Published date: January 20, 2017
Citation: Marafini I, Imeneo MG, Monteleone G (2017) The Role of Natural Killer Receptors in Celiac Disease. Immunome Res 13: 129. doi:10.4172/1745-7580.1000129
Copyright: © 2017 Monteleone G, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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.