Increased hepatic iron in mice lacking classical MHC class I molecules.

Elsa M Cardoso; Maria G Macedo; Pierre Rohrlich; Eduarda Ribeiro; Manuel T Silva; François A Lemonnier; Maria de Sousa

doi:10.1182/blood-2002-05-1565

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Increased hepatic iron in mice lacking classical MHC class I molecules.

Elsa M Cardoso·Maria G Macedo·Pierre Rohrlich·Eduarda Ribeiro·Manuel T Silva·François A Lemonnier·Maria de Sousa

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Abstract

Iron accumulation in the liver in hereditary hemochromatosis (HH) has been shown to be highly variable. Some studies point to the importance of major histocompatibility complex (MHC) class I (MHC-I) and CD8(+) cells as modifiers of iron overload. In this report, using mice knockout for H2K(b-/-) and H2D(b-/-) genes, it is demonstrated that lack of classical MHC-I molecules results in a spontaneous increase of nonheme 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.

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Animals CD8 Antigens CD8-Positive T-Lymphocytes DNA-Binding Proteins Ferritins Hemochromatosis Histocompatibility Antigens Class I Immunologic Deficiency Syndromes Iron Liver Male Mice Mice, Knockout Journal Article Research Support, Non-U.S. Gov't

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Elsa M Cardoso, Maria G Macedo, Pierre Rohrlich, Eduarda Ribeiro, Manuel T Silva, François A Lemonnier, Maria de Sousa. 2002-08-08. Increased hepatic iron in mice lacking classical MHC class I molecules.. https://doi.org/10.1182/blood-2002-05-1565

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