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Infection and Immunity, August 1999, p. 4143-4148, Vol. 67, No. 8
The Research Center for Protozoan Molecular
Immunology1 and Department of Veterinary
Physiology,
Received 11 January 1999/Returned for modification 26 February
1999/Accepted 27 May 1999
Babesia microti produces a self-limiting infection in
mice, and recovered mice are resistant to reinfection. In the present study, the role of T cells in protective immunity against challenge infection was examined. BALB/c mice which recovered from primary infection showed strong protective immunity against challenge infection. In contrast, nude mice which failed to control the primary
infection and were cured with an antibabesial drug did not show
protection against challenge infection. Treatment of immune mice with
anti-CD4 monoclonal antibody (MAb) diminished the protective immunity
against challenge infection, but treatment with anti-CD8 MAb had no
effect on the protection. Transfer of CD4+ T-cell-depleted
spleen cells resulted in higher parasitemia than transfer of
CD8+ T-cell-depleted spleen cells. A high level of gamma
interferon (IFN-
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.
Roles of CD4+ T Cells and Gamma
Interferon in Protective Immunity against Babesia microti
Infection in Mice
), which was produced by CD4+ T cells,
was observed for the culture supernatant of spleen cells from immune
mice, and treatment of immune mice with anti-IFN-
MAb partially
reduced the protection. Moreover, no protection against challenge
infection was found in IFN-
-deficient mice. On the other hand,
treatment of immune mice with MAbs against interleukin-2 (IL-2), IL-4,
or tumor necrosis factor alpha did not affect protective immunity.
These results suggest essential requirements for CD4+ T
cells and IFN-
in protective immunity against challenge infection with B. microti.
*
Corresponding author. Mailing address: The Research
Center for Protozoan Molecular Immunology, Obihiro University of
Agriculture and Veterinary Medicine, Obihiro, Hokkaido 080-8555, Japan.
Phone: 81-155-49-5641. Fax: 81-155-49-5643. E-mail:
igarcpmi{at}obihiro.ac.jp.
Infection and Immunity, August 1999, p. 4143-4148, Vol. 67, No. 8
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.
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