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Laboratories of
* Immunology,
Bacteriology and Medical Mycology, and
Virology, Istituto Superiore di Sanità, Rome, Italy;
Laboratory of Cytokine Signaling, Institut Pasteur, Paris, France; and
¶ Institute of Molecular Genetics, Centre National de la Recherche Scientifique, Unité Mixte de Recherche 5124, Montpellier, France
Type I IFN regulates different aspects of the immune response,
inducing a cell-mediated immunity. We have recently shown that the
infection of dendritic cells (DC) with Mycobacterium
tuberculosis (Mtb) induces IFN-
. In this work we have
monitored a rapid induction of IFN-
followed by the delayed
production of the IFN-1 and/or -13 subtypes. The Mtb infection
rapidly activates the NF-
B complex and stimulates the
phosphorylation of IFN regulatory factor (IRF)-3, events known to
induce IFN- expression in viral infection. In turn, the autocrine
production of IFN- induces the IFN-stimulated genes that contain
binding sites for activated STATs in their promoters. Among the
IFN-stimulated genes induced in DC through STAT activation are IRF-1
and IRF-7. The expression of IRF-1 appears to be dependent on the
sequential activation of NF-B and STAT-1. Once expressed, IRF-1 may
further stimulate the transcription of IFN-. Induction
of IRF-7 is also regulated at the transcriptional level through the
binding of phosphorylated STAT-1 and STAT-2, forming the IFN-stimulated
gene factor-3 complex. In turn, the IRF-1 and IRF-7 expression appears
to be required for the delayed induction of the IFN-1/13
genes. Although correlative, our results strongly support the
existence of a cascade of molecular events in Mtb-infected DC. Upon
infection, constitutively expressed NF-B and IRF-3 are activated and
likely contribute to the rapid IFN- expression. In turn,
IFN--induced IRF-1 and IRF-7 may cooperate toward induction of
IFN-1/13 if infection persists and these factors are
activated.
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