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,
,
*
Center for Immunology and Microbial Disease, Albany Medical College, Albany, NY 12208;
Laboratory of Immunology, Wadsworth Center, Albany, NY 12201;
Department of Biomedical Sciences, School of Public Health, State University of New York, Albany, NY 12201; and
§
Genetics Institute, Cambridge, MA 01810
Neonates are highly susceptible to infectious agents and are known
to display polarized expression of Th2-like cytokines and Abs. This
neonatal immune bias has important implications for the development of
vaccine strategies, particularly against viral infections. We now
report that coadministration of IL-12 and an influenza subunit vaccine
at birth enhances the protective efficacy of antiviral vaccination.
Immunization and treatment with IL-12 within 24 h of birth
resulted in elevated expression of IFN-
, IL-10, and IL-15 mRNA in
the spleens of newborn mice compared with animals exposed to vaccine
only. In addition, these animals showed dramatic increases in IFN--,
IL-2-, and IL-4-secreting cells, and in IgG2a Ab levels upon adult
challenge compared with mice primed with vaccine alone. Most
importantly, animals vaccinated and simultaneously treated with IL-12
at birth displayed enhanced survival after lethal challenge with
infectious influenza virus as adults compared with infected animals
that had been primed with vaccine alone. This augmented protection
required B cells and could be transferred to naive mice by immune
serum. Collectively, these results provide evidence that administration
of IL-12 to neonates induces a Th1-like response in newborns and
elicits protective antiviral immune memory.
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