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,
Departments of
*
Internal Medicine and
Microbiology, University of Iowa and the
Veterans Affairs Medical Center, Iowa City, IA 52242;
Department of Molecular and Cellular Biology, Harvard University, Cambridge, MA 02115; and the
¶
Department of Molecular Microbiology, Washington University, St. Louis, MO 63110
Protective immunity against Leishmania major
is provided by s.c. immunization with a low dose of L.
major promastigotes or with dihydrofolate-thymidylate synthase
gene locus (DHFR-TS) gene knockout L.
major organisms. Whether these vaccine strategies will protect
against infection with other Leishmania species that
elicit distinct immune responses and clinical syndromes is not known.
Therefore, we investigated protective immunity to Leishmania
chagasi, a cause of visceral leishmaniasis. In contrast to
L. major, a high dose s.c. inoculum of L.
chagasi promastigotes was required to elicit protective
immunity. Splenocytes from mice immunized with a high dose produced
significantly greater amounts of IFN-
and lower TGF-
than mice
immunized with a low dose of promastigotes. The development of
protective immunity did not require the presence of NK cells.
Protection was not afforded by s.c. immunization with either attenuated
L. chagasi or with L. major
promastigotes, and s.c. L. chagasi did not protect
against infection with L. major. Subcutaneous
immunization with DHFR-TS gene knockouts derived from
L. chagasi, L. donovani, or L. major did
not protect against L. chagasi infection. We conclude
that s.c. inoculation of high doses of live L. chagasi
causes a subclinical infection that elicits protective immune responses
in susceptible mice. However, L. chagasi that have been
attenuated either by long-term passage or during the raising of
recombinant gene knockout organisms do not elicit protective immunity,
either because they fail to establish a subclinical infection or
because they no longer express critical antigenic
epitopes.
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