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Increased hepatic iron in mice lacking classical MHC class I molecules.
- Source :
-
Blood [Blood] 2002 Dec 01; Vol. 100 (12), pp. 4239-41. Date of Electronic Publication: 2002 Aug 08. - Publication Year :
- 2002
-
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.
- 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
Subjects
Details
- Language :
- English
- ISSN :
- 0006-4971
- Volume :
- 100
- Issue :
- 12
- Database :
- MEDLINE
- Journal :
- Blood
- Publication Type :
- Academic Journal
- Accession number :
- 12393413
- Full Text :
- https://doi.org/10.1182/blood-2002-05-1565