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Gliadin Regulates the NK-Dendritic Cell Cross-Talk by HLA-E Surface Stabilization¹

Giuseppe Terrazzano^2,*, Michela Sica^*, Carmen Gianfrani, Giuseppe Mazzarella, Francesco Maurano, Beatrice De Giulio, Sophie de Saint-Mezard, Delia Zanzi, Luigi Maiuri^¶, Marco Londei^¶, Bana Jabri, Riccardo Troncone, Salvatore Auricchio, Serafino Zappacosta^* and Ennio Carbone^*,||,#,**

^* Department of Cellular and Molecular Biology and Pathology, University Federico II, Naples, Italy; Institute of Food Science and Technology, Consiglio Nazionale delle Ricerche, Avellino, Italy; Department of Pathology, University of Chicago, Chicago, IL 60607; Department of Pediatrics and European Laboratory for the Investigation of Food-Induced Diseases, University Federico II, Naples, Italy; ^¶ Institute of Child Health, University College London, London, United Kingdom; ^|| Department of Experimental and Clinical Medicine University "Magna Graecia," Catanzaro, Italy; ^# Research Center for Studies of Integrative Recognition in the Immune System, Karolinska Institutet, Stockholm, Sweden; and ^** Microbiology and Tumorbiology Centre, Karolinska Institutet, Stockholm, Sweden

We analyzed the autologous NK cell interaction with gliadin-presenting dendritic cells. Gliadin is the known Ag priming the celiac disease (CD) pathogenesis. We demonstrate that gliadin prevents immature dendritic cells (iDCs) elimination by NK cells. Furthermore, cooperation between human NK cells-iDCs and T cells increases IFN- production of anti-gliadin immune response. Gliadin fractions were analyzed for their capability to stabilize HLA-E molecules. The and fractions conferred the protection from NK cell lysis to iDCs and increased their HLA-E expression. Gliadin pancreatic enzyme digest and a peptide derived from gliadin increased HLA-E levels on murine RMA-S/HLA-E-transfected cells. Analysis of HLA-E expression in the small intestinal mucosa of gluten-containing diet celiac patients and organ culture experiments confirmed the in vitro data.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ This work was supported by grants from the Italian Association for Celiac Disease, the Italian Association for Cancer Research, and the National Institutes of Health.

² Address correspondence and reprint requests to Dr. Giuseppe Terrazzano, Department of Cellular and Molecular Biology and Pathology, University Federico II, Naples, Italy. E-mail address: terrazza{at}unina.it

³ Abbreviations used in this paper: CD, celiac disease; BFA, brefeldin A; DC, dendritic cell; g-iTCL, gliadin-restricted intestinal T cell line; iDC, immature DC; KIR, killer Ig-like receptor; MHC-I, MHC class I; PT, peptic-tryptic digest; PTCE, pepsine-trypsin-chymotrypsin-elastasis digest; RT, room temperature.

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