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Prepublished online as a Blood First Edition Paper on August 8, 2002; DOI 10.1182/blood-2002-05-1565.
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Blood, 1 December 2002, Vol. 100, No. 12, pp. 4239-4241
BRIEF REPORT
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, and
Maria de
Sousa
From Molecular Immunology and Immunobiology, Institute
for Molecular and Cell Biology; Instituto Superior de Ciências da
Saúde-Norte; Molecular Immunology and Pathology, Instituto de
Ciências Biomédicas Abel Salazar, Oporto, Portugal;
Unité d'Immunité Cellulaire Antivirale, Institut Pasteur,
Paris, France.
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.
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