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Production and Innate Immunity During Listeria monocytogenes Infection in the Absence of NK Cells1
,
*
Institut National de la Santé et de la Recherche Médicale Unit 429, Hôpital Necker-Enfants Malades, Paris, France;
Max Planck Institute for Immunobiology, Freiburg, Germany; and
University of Cape Town, Cape Town, South Africa
NK cells are believed to play a mandatory role during the early
phases of Listeria monocytogenes infection by producing
IFN-
, which is required for the activation of macrophage effector
functions. Mice deficient in the common cytokine receptor -chain
(c-/-), which completely lack NK cells,
were used to examine whether NK cells were essential for resistance to
Listeria infection in vivo. Surprisingly, infected
c-/- mice showed normal innate immunity
and macrophage responses against sublethal Listeria
infection 2 days postinfection. At this time point,
c-/- mice showed increased blood IFN-
levels compared with those in noninfected controls, demonstrating an
NK-independent source of IFN-, which explains early resistance.
Listeria-infected c-/- x
recombinase-activating gene-2-/- double-deficient mice
were unable to produce IFN- and were highly susceptible to L.
monocytogenes. Since T cells, but not B cells, are major
IFN- producers, and c-/- T cells were
found to be efficient IFN- producers in vitro, we conclude from
these results that T cells functionally replace NK cells for the early
IFN- production that is necessary for activating the innate immune
system following infection with L. monocytogenes. This
novel observation in listeriosis underscores how the adaptive immune
response can maintain and influence innate
immunity.
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