Development of experimental cerebral malaria is independent of IL-23 and IL-17

Hidekazu Ishida, Chikako Matsuzaki-Moriya, Takashi Imai, Kunio Yanagisawa, Yoshihisa Nojima, Kazutomo Suzue, Makoto Hirai, Yoichiro Iwakura, Akihiko Yoshimura, Shinjiro Hamano, Chikako Shimokawa, Hajime Hisaeda

Research output: Contribution to journalArticlepeer-review

30 Citations (Scopus)


Cerebral malaria (CM) is the most severe complication of Plasmodium infection. Although inappropriate immune responses to Plasmodium falciparum are reported as the major causes of CM, the precise mechanisms for development remain unclear. IL-23 and IL-17 have critical roles in the onset of autoimmunity and inflammatory diseases triggered by microbial infections. Thus, we investigated the influence of IL-23 and IL-17 on experimental CM (ECM) using Plasmodium berghei ANKA infection of C57BL/6 mice. Both IL-23 deficient mice and wild-type (WT) mice developed ECM. IL-17 deficient mice also developed ECM, while IL-17 producing cells other than CD4 + T cells (Th17) were increased in WT mice that developed ECM. In conclusion, this study showed that IL-23 and IL-17 are not involved in ECM development.

Original languageEnglish
Pages (from-to)790-795
Number of pages6
JournalBiochemical and Biophysical Research Communications
Issue number4
Publication statusPublished - 2010 Nov 26


  • Cerebral malaria
  • IL-17
  • IL-23
  • Immune responses
  • Malaria

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology


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