Increased hepatic iron in mice lacking classical MHC class I molecules
Copyright policy )Increased hepatic iron in mice lacking classical MHC class I molecules
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 H2Kb−/−and H2Db−/− 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.
Male, Mice, Knockout, CD8 Antigens, Iron, Histocompatibility Antigens Class I, Immunologic Deficiency Syndromes, CD8-Positive T-Lymphocytes, DNA-Binding Proteins, Mice, Liver, Ferritins, Animals, Hemochromatosis
Male, Mice, Knockout, CD8 Antigens, Iron, Histocompatibility Antigens Class I, Immunologic Deficiency Syndromes, CD8-Positive T-Lymphocytes, DNA-Binding Proteins, Mice, Liver, Ferritins, Animals, Hemochromatosis
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