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Clinical Immunology Section, Laboratory of Clinical Investigation,
Laboratory of Allergic Diseases,
Laboratory of Parasitic Diseases, and
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Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892;
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Institut de Pharmacologie Moléculaire et Cellulaire, Centre National de la Recherche Scientifique (CNRS), Valbonne, France;
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Howard Hughes Medical Institute-National Institutes of Health Medical Research Scholars,
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University of California, San Francisco, CA 94143; and
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Howard Hughes Medical Institute, Bethesda, MD 20892
Protective immunity against Leishmania major
generated by DNA encoding the LACK (Leishmania homologue
of receptor for activated C kinase) Ag has been shown to be more
durable than vaccination with LACK protein plus IL-12. One mechanism to
account for this may be the selective ability of DNA vaccination to
induce CD8+ IFN-
-producing T cells. In this regard, we
previously reported that depletion of CD8+ T cells in LACK
DNA-vaccinated mice abrogated protection when infectious challenge was
done 2 wk postvaccination. In this study, we extend these findings to
study the mechanism by which CD8+ T cells induced by LACK
DNA vaccination mediate both short- and long-term protective immunity
against L. major. Mice vaccinated with LACK DNA and
depleted of CD8+ T cells at the time of vaccination or
infection were unable to control infection when challenge was done 2 or
12 wk postvaccination. Remarkably, it was noted that depletion of
CD8+ T cells in LACK DNA-vaccinated mice was associated
with a striking decrease in the frequency of LACK-specific
CD4+ IFN--producing T cells both before and after
infection. Moreover, data are presented to suggest a mechanism by which
CD8+ T cells exert this regulatory role. Taken together,
these data provide additional insight into how Th1 cells are generated
and sustained in vivo and suggest a potentially novel immunoregulatory
role for CD8+ T cells following DNA
vaccination.
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