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* Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, and
Dermatology Branch, Division of Clinical Sciences, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892
Standard murine models of cutaneous leishmaniasis, involving s.c.
inoculation of large numbers of Leishmania major
promastigotes, have not supported an essential role for
CD8+ T cells in the control of primary infection. Recently,
a L. major model combining two main features of natural
transmission, low parasite dose and inoculation into a dermal site, has
been established in resistant C57BL/6 mice. In the present studies,
C57BL/6 mice with CD8+ T cell deficiencies, including
CD8-/- and CD8-depleted mice, failed to control the
growth of L. major following inoculation of 100
metacyclic promastigotes into the ear dermis. The resulting dermal
pathology was minor and delayed. Lesion formation in wild-type mice was
coincident with the killing of parasites in the inoculation site. Both
events were associated with the accumulation of CD8+ T
lymphocytes in the skin and with the capacity of CD8+ T
cells recovered from draining lymph nodes or infected dermis to release
IFN-
following coculture with infected dendritic cells.
Reconstitution of resistance to L. major in
RAG-/- mice using T cells from naive donors was optimal
when both CD4+ and CD8+ T cells were
transferred. Primed CD8+ T lymphocytes obtained from
C57BL/6 mice during the acute stage of infection were able to mediate
both pathology and immunity when transferred alone. The low dose,
intradermal challenge model reveals that CD8+ T cells play
an essential role in both pathogenesis of and immunity to primary
infection with L. major in the
skin.
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