1. Increased hepatic iron in mice lacking classical MHC class I molecules.
- Author
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Cardoso EM, Macedo MG, Rohrlich P, Ribeiro E, Silva MT, Lemonnier FA, and de Sousa M
- Subjects
- Animals, CD8 Antigens genetics, CD8 Antigens physiology, CD8-Positive T-Lymphocytes, DNA-Binding Proteins genetics, DNA-Binding Proteins physiology, Ferritins metabolism, Hemochromatosis etiology, Hemochromatosis genetics, Histocompatibility Antigens Class I genetics, Liver cytology, Male, Mice, Mice, Knockout, Histocompatibility Antigens Class I physiology, Immunologic Deficiency Syndromes metabolism, Iron metabolism, Liver metabolism
- 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.
- Published
- 2002
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