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Interleukin-12-Dependent Mechanisms in the Clearance of Blood-Stage Murine Malaria Parasite Plasmodium berghei XAT, an Attenuated Variant of P. berghei NK65
Takayuki Yoshimoto, Toshihiko Yoneto, Seiji Waki and Hideo Nariuchi
The Journal of Infectious Diseases
Vol. 177, No. 6 (Jun., 1998), pp. 1674-1681
Published by: Oxford University Press
Stable URL: http://www.jstor.org/stable/30108890
Page Count: 8
You can always find the topics here!Topics: Infections, Parasites, Messenger RNA, Inoculation, Parasitemia, T lymphocytes, Spleen, Parasite hosts, Cytokines, Malaria
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The mechanism of development of host resistance to blood-stage malarial infection was studied by use of an irradiation-induced attenuated variant, Plasmodium berghei XAT, obtained from a lethal strain, P. berghei NK65. The infection enhanced mRNA expression of interleukin (IL)-12 p40 and also of interferon (IFN)-γ, IL-4, IL-10, and cytokine-inducible nitric oxide synthase (iNOS) in spleen. Treatment of these mice with anti-IL-12 or anti-IFN-γ led to the progression of parasitemia and fatal outcome. Anti-IL-12 treatment significantly reduced the secretion and mRNA expression of IFN-γ and greatly diminished the augmentation of iNOS mRNA expression. In addition, recombinant IL-12 administration delayed the onset of parasitemia because of the enhanced IFN-γ production. These results suggest that blood-stage P. berghei XAT infection induces IL-12 production, which is important for the development of host resistance via IFN-γ production.
The Journal of Infectious Diseases © 1998 Oxford University Press