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Invariant V14⁺ NKT Cells Participate in the Early Response to Enteric Listeria monocytogenes Infection¹

Thomas Ranson^2,*, Søren Bregenholt^2,3,*, Agnes Lehuen, Olivier Gaillot, Maria C. Leite-de-Moraes, André Herbelin, Patrick Berche and James P. Di Santo^4,*

^* 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 V14⁺ NKT cells are a specialized CD1-reactive T cell subset implicated in innate and adaptive immunity. We assessed whether V14⁺ 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 V14⁺ NKT cells in C57BL/6 mice were early producers of IFN- (but not IL-4) after L. monocytogenes infection. Adoptive transfer of V14⁺ NKT cells derived from TCR° V14-J18 transgenic (TCR°V14Tg) mice into alymphoid Rag°_c° mice demonstrated that V14⁺ 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 J18° mice, but not TCR° or TCR°V14Tg mice, were able to mount adaptive responses to L. monocytogenes. These data demonstrate that V14⁺ 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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