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T Cells Are Sufficient for Innate and Adaptive Immunity Against Enteric Listeria monocytogenes1
*
Unité des Cytokines et Développement Lymphoïde, Institut Pasteur, 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
University of Cape Town, Cape Town, South Africa
We have begun to dissect the cellular requirements for generation
of immunity against enteric infection by Listeria
monocytogenes using a novel T- B-
NK- mouse strain (mice double deficient for the common
cytokine receptor 
-chain (c) and the
recombinase-activating gene-2 (RAG2/c mice). Initial
experiments showed that C57BL/6 mice and alymphoid
RAG2/c mice had similar kinetics of bacterial
accumulation in the spleen, liver, and brain early after intragastric
L. monocytogenes infection (up to day 3), calling into
question the physiologic role of gut-associated lymphoid cells during
the passage of this enterobacterium into the host. However, in contrast
to C57BL/6 mice, RAG2/c mice rapidly succumbed to
disseminated infection by day 7. Polyclonal lymph node CD4+
and CD8+ 
T cells were able to confer
RAG2/c mice with long-lasting protection against enteric
L. monocytogenes infection in the absence of 
T,
NK, and NK-T cells. Moreover, these T-reconstituted
RAG2/c mice produced IFN- at levels comparable to
C57BL/6 mice in response to L. monocytogenes both in
vitro and in vivo. Protection was IFN- dependent, as
RAG2/c mice reconstituted with IFN--deficient
T cells were unable to control enteric L. monocytogenes
infection. Furthermore, T cell-reconstituted
RAG2/c mice were able to mount memory responses when
challenged with lethal doses of L. monocytogenes. These
data suggest that NK, NK-T, T, and B cells are functionally
redundant in the immunity against oral L. monocytogenes
infection, and that in their absence T cells are able to mediate
the early IFN- production required for both innate and adaptive
immunity.
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