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From the * Laboratory for Immunological Research, Schering-Plough, Dardilly, France; and Secondary infections due to a marked immunosuppression have long been recognized as a major cause of the high morbidity and mortality rate associated with acute measles. The mechanisms underlying the inhibition of cell-mediated immunity are not clearly understood but dysfunctions of monocytes as antigen-presenting cells (APC) are implicated. In this report, we
demonstrate that measles virus (MV) replicates weakly in the resting dendritic cells (DC) as in
lipopolysaccharide-activated monocytes, but intensively in CD40-activated DC. The interaction of MV-infected DC with T cells not only induces syncytia formation where MV undergoes massive replication, but also leads to an impairment of DC and T cell function and cell
death. CD40-activated DC decrease their capacity to produce interleukin (IL) 12, and T cells
are unable to proliferate in response to MV-infected DC stimulation. A massive apoptosis of
both DC and T cells is observed in the MV pulsed DC-T cell cocultures. This study suggests
that DC represent a major target of MV. The enhanced MV replication during DC-T cell interaction, leading to an IL-12 production decrease and the deletion of DC and T cells, may be
the essential mechanism of immunosuppression induced by MV.
Immunobiologie Moléculaire, Laboratoire de Biologie Cellulaire et Moléculaire de l'Ecole Normale
Supérieure de Lyon, Lyon, France
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