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Immunobiologie Fondamentale et Clinique, Institut National de la Santé et de la Recherche Médicale U503, Ecole Normale Supérieur Lyon, Lyon, France;
Biologie des Cellules Dendritiques Humaines, Institut National de la Santé et de la Recherche Médicale E 9908, Etablissement de Transfusion Sanguine Strasbourg, Strasbourg, France;
Immunité et infections virales, Faculté de médecine Laennec, IVMC-Centre National de la Recherche Scientifique-Université Claude Bernard Lyon Unité Mixte de Recherche 5537, Lyon, France; and
§
Développement Normal et Pathologique du Système Immunitaire, Institut National de la Santé et de la Recherche Médicale U429, Hôpital Necker-Enfants Malades, Paris, France
Measles virus (MV) infection induces a profound immunosuppression
responsible for a high rate of mortality in malnourished children. MV
can encounter human dendritic cells (DCs) in the respiratory mucosa or
in the secondary lymphoid organs. The purpose of this study was to
investigate the consequences of DC infection by MV, particularly
concerning their maturation and their ability to generate
CD8+ T cell proliferation. We first show that MV-infected
Langerhans cells or monocyte-derived DCs undergo a maturation process
similarly to the one induced by TNF-
or LPS, respectively. CD40
ligand (CD40L) expressed on activated T cells is shown to induce
terminal differentiation of DCs into mature effector DCs. In contrast,
the CD40L-dependent maturation of DCs is inhibited by MV infection, as
demonstrated by CD25, CD69, CD71, CD40, CD80, CD86, and CD83 expression
down-regulation. Moreover, the CD40L-induced cytokine pattern in DCs is
modified by MV infection with inhibition of IL-12 and IL-1/ß and
induction of IL-10 mRNAs synthesis. Using peripheral blood lymphocytes
from CD40L-deficient patients, we demonstrate that MV infection of DCs
prevents the CD40L-dependent CD8+ T cell proliferation. In
such DC-PBL cocultures, inhibition of CD80 and CD86 expression on DCs
was shown to require both MV replication and CD40 triggering. Finally,
for the first time, MV was shown to inhibit tyrosine-phosphorylation
level induced by CD40 activation in DCs. Our data demonstrate that MV
replication modifies CD40 signaling in DCs, thus leading to impaired
maturation. This phenomenon could play a pivotal role in MV-induced
immunosuppression.
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