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14+ NKT Cells Participate in the Early Response to Enteric Listeria monocytogenes Infection1





* Unité des Cytokines et Développement Lymphoïde, Institut National de la Santé et de la Recherche Médicale Unité 668, Institut Pasteur, Paris, France;
Institut National de la Santé et de la Recherche Médicale Unité 561, Hopital Cochin-Saint Vincent de Paul, Paris, France;
Laboratoire de Microbiologie, Institut National de la Santé et de la Recherche Médicale Unité 411, Faculté de Médecine Necker-Enfants Malades, Paris, France; and
Centre National de la Recherche Scientifique Unité Mixte Recherche 8147, Paris V, Institut de Recherche Necker-Enfants Malades, Paris, France
Invariant V
14+ NKT cells are a specialized CD1-reactive T cell subset implicated in innate and adaptive immunity. We assessed whether V
14+ NKT cells participated in the immune response against enteric Listeria monocytogenes infection in vivo. Using CD1d tetramers loaded with the synthetic lipid
-galactosylceramide (CD1d/
GC), we found that splenic and hepatic V
14+ NKT cells in C57BL/6 mice were early producers of IFN-
(but not IL-4) after L. monocytogenes infection. Adoptive transfer of V
14+ NKT cells derived from TCR
° V
14-J
18 transgenic (TCR
°V
14Tg) mice into alymphoid Rag°
c° mice demonstrated that V
14+ NKT cells were capable of providing early protection against enteric L. monocytogenes infection with systemic production of IFN-
and reduction of the bacterial burden in the liver and spleen. Rechallenge experiments demonstrated that previously immunized wild-type and J
18° mice, but not TCR
° or TCR
°V
14Tg mice, were able to mount adaptive responses to L. monocytogenes. These data demonstrate that V
14+ NKT cells are able to participate in the early response against enteric L. monocytogenes through amplification of IFN-
production, but are not essential for, nor capable of, mediating memory responses required to sterilize the host.
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