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Overexpression of Cellular Prion Protein Induces an Antioxidant Environment Altering T Cell Development in the Thymus¹

Evelyne Jouvin-Marche^2,*, Valérie Attuil-Audenis^2,*, Catherine Aude-Garcia^2,*, Walid Rachidi^3,, Mark Zabel, Valérie Podevin-Dimster, Carole Siret^||, Christoph Huber, Marianne Martinic^¶, Jacqueline Riondel, Christian L. Villiers^*, Alain Favier, Philippe Naquet^||, Jean-Yves Cesbron and Patrice N. Marche^4,*

^* Laboratoire d’Immunochimie, Commissariat à l’Energie Atomique, Institut National de la Santé et de la Recherche Médicale Unité 548, Université J. Fourier, Grenoble, France; Laboratoire de Biologie du Stress Oxydant and Transmission et Pathogénèse des Maladies à Prions, Centre National de la Recherche Scientifique FRE 2685, Université J. Fourier, La Tronche, France; Neuropathology Institute, University Hospital of Zurich and ^¶ Institute of Experimental Immunology, Zurich, Switzerland; and ^|| CIML, Centre National de la Recherche Scientifique-Institut National de la Santé et de la Recherche Médicale-Université de la Méditerranée, Parc scientifique de Luminy, Marseille, France

Cellular prion protein (PrP^C) is an ubiquitously expressed glycoprotein whose roles are still widely discussed, particularly in the field of immunology. Using TgA20- and Tg33-transgenic mice overexpressing PrP^C, we investigated the consequences of this overexpression on T cell development. In both models, overexpression of PrP^C induces strong alterations at different steps of T cell maturation. On TgA20 mice, we observed that these alterations are cell autonomous and lead to a decrease of T cells and a concomitant increase of T cell numbers. PrP^C has been shown to bind and chelate copper and, interestingly, under a copper supplementation diet, TgA20 mice presented a partial restoration of the T cell development, suggesting that PrP^C overexpression, by chelating copper, generates an antioxidant context differentially impacting on and T cell lineage.

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The JI 2006 176: 3289-3290. [Full Text]