IL-23 protection against Plasmodium berghei infection in mice is partially dependent on IL-17 from macrophages

Hidekazu Ishida, Takashi Imai, Kazutomo Suzue, Makoto Hirai, Tomoyo Taniguchi, Akihiko Yoshimura, Yoichiro Iwakura, Hiroko Okada, Tomohisa Suzuki, Chikako Shimokawa, Hajime Hisaeda

研究成果: Article査読

27 被引用数 (Scopus)


Although IL-12 is believed to contribute to protective immune responses, the role played by IL-23 (a member of the IL-12 family) in malaria is elusive. Here, we show that IL-23 is produced during infection with Plasmodium berghei NK65. Mice deficient in IL-23 (p19KO) had higher parasitemia and died earlier than wild-type (WT) controls. Interestingly, p19KO mice had lower numbers of IL-17-producing splenic cells than their WT counterparts. Furthermore, mice deficient in IL-17 (17KO) suffered higher parasitemia than the WT controls, indicating that IL-23-mediated protection is dependent on induction of IL-17 during infection. We found that macrophages were responsible for IL-17 production in response to IL-23. We observed a striking reduction in splenic macrophages in the p19KO and 17KO mice, both of which became highly susceptible to infection. Thus, IL-17 appears to be crucial for maintenance of splenic macrophages. Adoptive transfer of macrophages into macrophage-depleted mice confirmed that macrophage-derived IL-17 is required for macrophage accumulation and parasite eradication in the recipient mice. We also found that IL-17 induces CCL2/7, which recruit macrophages. Our findings reveal a novel protective mechanism whereby IL-23, IL-17, and macrophages reduce the severity of infection with blood-stage malaria parasites.

ジャーナルEuropean Journal of Immunology
出版ステータスPublished - 2013 10月

ASJC Scopus subject areas

  • 免疫アレルギー学
  • 免疫学


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