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

Abstract

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.

• Authors: 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
• Journal: Biochemical and biophysical research communications (Biochem Biophys Res Commun) Vol. 402 Issue 4 Pg. 790-5 (Nov 26 2010) ISSN: 1090-2104 [Electronic] United States
• PMID: 21036146 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
• Copyright: Copyright © 2010 Elsevier Inc. All rights reserved.

Chemical References

• Interleukin-17
• Interleukin-23

Topics

• Animals
• Disease Models, Animal
• Female
• Interleukin-17 (genetics, metabolism)
• Interleukin-23 (genetics, metabolism)
• Malaria, Cerebral (genetics, immunology)
• Male
• Mice
• Mice, Inbred C57BL
• Mice, Knockout
• Plasmodium falciparum