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McGill University, Department of Experimental Medicine, Montreal General Hospital Research Institute, Montreal, Quebec, Canada; and
Central University of Venezuela, Faculty of Medicine, Institute of Immunology, Caracas, Venezuela
The natural resistance associated macrophage protein 1
(Nramp1) gene determines the ability of murine
macrophages to control infection with a group of intracellular
pathogens, including Salmonella typhimurium,
Leishmania donovani, and Mycobacterium
bovis bacillus Calmette-Guérin (BCG). The expression of
the resistant allele of the Nramp1 gene in murine
macrophages is associated with a more efficient expression of several
macrophage activation-associated genes, including class II MHC loci. In
this study, we investigated the molecular mechanisms involved in
IFN-
-induced MHC class II expression in three types of macrophages:
those expressing a wild-type allele of the Nramp1 gene
(B10R and 129/M
), those carrying a susceptible form of the
Nramp1 gene (B10S), and those derived from
129-Nramp1-knockout mice (129/Nramp1-KO).
Previously, we published results showing that Ia protein expression is
significantly higher in the IFN--induced B10R macrophages, compared
with its susceptible counterpart. In this paper, we also show that the
higher expression of Ia protein in B10R cells is associated with higher
I-Aß mRNA expression, which correlates with a higher
level of IFN--induced phosphorylation of the STAT1-
protein and
subsequently with elevated expression of class II transactivator
(CIITA) mRNA, compared with B10S. Furthermore, we demonstrate that the
infection of macrophages with M. bovis BCG results in a
down-regulation of CIITA mRNA expression and, consequently, in the
inhibition of Ia induction. Therefore, our data explain, at least in
part, the molecular mechanism involved in the inhibition of
I-Aß gene expression in M. bovis
BCG-infected macrophages activated with IFN-.
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