Effects of in vino administration of anti-IL-10 or anti-IFN-γ monoclonal antibody on the host defense mechanism against Plasmodium yoelii yoelii infection

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  • KOBAYASHI Fumie
    Department of Tropical Diseases and Parasitology, Kyorin University School of Medicine, Mitaka, Tokyo 181-8611, Japan
  • ISHIDA Hiroshi
    Department of Internal Medicine and Clinical Research Center, Utano National Hospital, Kyoto 616-8255, Japan
  • MATSUI Toshihiro
    Department of Tropical Diseases and Parasitology, Kyorin University School of Medicine, Mitaka, Tokyo 181-8611, Japan
  • TSUJI Moriyasu
    Department of Tropical Diseases and Parasitology, Kyorin University School of Medicine, Mitaka, Tokyo 181-8611, Japan

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タイトル別名
  • Effects of in vivo Administration of Anti-IL-10 or Anti-IFN-.GAMMA. Monoclonal Antibody on the Host Defense Mechanism against Plasmodium yoelii yoelii Infection.
  • Effects of in vino administration of anti IL 10 or anti IFN ガンマ monoclonal antibody on the host defense mechanism against Plasmodium yoelii yoelii infection
  • Effects of in vivo administration of anti–IL–10 or anti–IFN–γ monoclonal antibody on the host defense mechanism against Plasmodium yoelii infection

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Our previous reports indicated that C57BL/6 mice infected with a lethal variant of Plasmodium yoelii 17X (P. yoelii 17XL) produced high levels of interleukin 10 (IL-10) and interferon-γ (IFN-γ) while mice infected with the nonlethal variant of the parasite did not produce detectable levels of IL-10. In the present study, the involvement of IL-10 and IFN-γ in exacerbation or regulation of blood-stage malaria was investigated by using the lethal variant of P. yoelii 17XL and monoclonal antibodies (mAb) against the cytokines. C57BL/6 mice were injected intraperitoneally with a neutralizing anti-IL-10 mAb or anti-IFN-γ mAb after inoculation with P. yoelii 17XL. Treatment of mice with anti-IL-10 mAb resulted in substantial prolongation of survival and 60% of treated mice survived while 100% of control mice died by day 11. On the contrary, treatment of mice with anti-IFN-γ mAb exacerbated infection and all mice died after an earlier period than those treated with normal rat Ig. No differences in parasitemias were found between treated and untreated mice. To elucidate the involvement of nitric oxide in the host protection or exacerbation, mice were treated with aminoguanidine, an inhibitor of nitric oxide synthetase, after inoculation of P. yoelii 17XL. Neither mortality nor parasitemia was influenced by the treatment. These results indicate that an IFN-γ response is associated with protective immunity in mice infected with P. yoelii 17XL, while an IL-10 response is associated with disease exacerbation during the infection.

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