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241 m/s n° 3, vol. 32, mars 2016 DOI : 10.1051/medsci/20163203005 4. Sinclair LV, Rolf J, Emslie E, et al. Control of aminoacid transport by antigen receptors coordinates the metabolic reprogramming essential for T cell differentiation. Nat Immunol 2013 ; 14 : 500-8. 5. Das A, Hoare M, Davies N, et al. Functional skewing of the global CD8 T cell population in chronic hepatitis B virus infection. J Exp Med 2008 ; 205 : 2111-24. 6. Gabrilovich DI, Ostrand-Rosenberg S, Bronte V. Coordinated regulation of myeloid cells by tumours. Nat Rev Immunol 2012 ; 12 : 253-68. 7. Chen S, Akbar SMF, Abe M, et al. Immunosuppressive functions of hepatic myeloid-derived suppressor cells of normal mice and in a murine model of chronic hepatitis B virus. Clin Exp Immunol 2011 ; 166 : 134-42. 8. Ferrari C. HBV and the immune response. Liver Int 2015 ; 35 (suppl 1) : 121-8. 9. Wieland S, Thimme R, Purcell RH, et al. Genomic analysis of the host response to hepatitis B virus infection. Proc Natl Acad Sci USA 2004 ; 101 : 6669-74. 10. Busca A, Kumar A. Innate immune responses in hepatitis B virus (HBV) infection. Virol J 2014 ; 11 : 22. 11. Lucifora J, Xia Y, Reisinger F, et al. Dégradation spécifique de l’ADN nucléaire responsable de la persistance du virus de l’hépatite B. Med Sci (Paris) 2014 ; 30 : 724-6. la réactivation du système immunitaire chez les patients infectés. ‡ gMDSCs act as metabolic regulators of hepatitis B virus immunopathology

Le facteur nétrine-1 régule la reprogrammation cellulaire vers l’état pluripotent