| First Author | Cardoso EM | Year | 2002 |
| Journal | Blood | Volume | 100 |
| Issue | 12 | Pages | 4239-41 |
| PubMed ID | 12393413 | Mgi Jnum | J:115559 |
| Mgi Id | MGI:3691927 | Doi | 10.1182/blood-2002-05-1565 |
| Citation | Cardoso EM, et al. (2002) Increased hepatic iron in mice lacking classical MHC class I molecules. Blood 100(12):4239-41 |
| abstractText | 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. |
