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Prepublished online as a Blood First Edition Paper on August 8, 2002; DOI 10.1182/blood-2002-05-1565. This Article Full Text (PDF) All Versions of this Article: 2002-05-1565v1 100/12/4239    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Cardoso, E. M Articles by de Sousa, M. Search for Related Content PubMed PubMed Citation Articles by Cardoso, E. M Articles by de Sousa, M. Social Bookmarking                   What's this? Submitted May 29, 2002 Accepted July 8, 2002 Increased hepatic iron in mice lacking classical MHC-class I molecules Elsa M Cardoso, Maria G Macedo, Pierre Rohrlich, Eduarda Ribeiro, Manuel T Silva, Francois A Lemonnier, and Maria de Sousa* Molecular Immunology, IBMC, Oporto, Portugal; ISCS-N, Oporto, Portugal Molecular Immunology, IBMC, Oporto, Portugal Unite d Immunite Cellulaire Antivirale, Institut Pasteur, Paris, France Molecular Immunology and Pathology, ICBAS, Oporto, Portugal Immunobiology, IBMC, Oporto, Portugal Molecular Immunology, IBMC, Oporto, Portugal; Molecular Immunology and Pathology, ICBAS, Oporto, Portugal * Corresponding author; email: mdesousa{at}ibmc.up.pt. Iron accumulation in the liver in hereditary hemochromatosis (HH) has been shown to be highly variable. Some studies point to the importance of MHC class I (MHC-I) and CD8+ cells as modifiers of iron overload. In this, report using mice knockout for H2Kb-/- and H2Db-/- genes, it is demonstrated that lack of classical MHC-I molecules results in a spontaneous increase of non-heme iron content in the liver (mainly located in the hepatocytes), when compared to wild type mice. In CD8-/- and Rag2-/- mice no spontaneous hepatic iron accumulation was observed. These results demonstrate for the first time that classical MHC-I molecules could be involved in the regulation of iron metabolism and contribute to the established genotype/phenotype discrepancies seen in HH. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: N. C. Andrews Forging a field: the golden age of iron biology Blood, July 15, 2008; 112(2): 219 - 230. [Full Text] [PDF] M. Constante, W. Jiang, D. Wang, V.-A. Raymond, M. Bilodeau, and M. M. Santos Distinct requirements for Hfe in basal and induced hepcidin levels in iron overload and inflammation Am J Physiol Gastrointest Liver Physiol, August 1, 2006; 291(2): G229 - G237. [Abstract] [Full Text] [PDF] H. Makui, R. J. Soares, W. Jiang, M. Constante, and M. M. Santos Contribution of Hfe expression in macrophages to the regulation of hepatic hepcidin levels and iron loading Blood, September 15, 2005; 106(6): 2189 - 2195. [Abstract] [Full Text] [PDF] P. S. Rohrlich, N. Fazilleau, F. Ginhoux, H. Firat, F. Michel, M. Cochet, N. Laham, M. P. Roth, S. Pascolo, F. Nato, et al. From The Cover: Direct recognition by {alpha}{beta} cytolytic T cells of Hfe, a MHC class Ib molecule without antigen-presenting function PNAS, September 6, 2005; 102(36): 12855 - 12860. [Abstract] [Full Text] [PDF] C. J. Miranda, H. Makui, N. C. Andrews, and M. M. Santos Contributions of {beta}2-microglobulin-dependent molecules and lymphocytes to iron regulation: insights from HfeRag1-/- and {beta}2mRag1-/- double knock-out mice Blood, April 1, 2004; 103(7): 2847 - 2849. [Abstract] [Full Text] [PDF]

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