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Development of experimental cerebral malaria is independent of IL-23 and IL-17 |
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| Authors: | Ishida Hidekazu Matsuzaki-Moriya Chikako Imai Takashi Yanagisawa Kunio Nojima Yoshihisa Suzue Kazutomo Hirai Makoto Iwakura Yoichiro Yoshimura Akihiko Hamano Shinjiro Shimokawa Chikako Hisaeda Hajime |
| Institution: | a Department of Microbiology and Immunology, Graduate School of Medical Sciences, Kyushu University, Fukuoka 812-8582, Japan b Department of Parasitology, Gunma University, Graduate School of Medicine, Gunma 371-8511, Japan c Department of Medicine and Clinical Science, Gunma University, Graduate School of Medicine, Gunma 371-8511, Japan d Center for Experimental Medicine, Institute of Medical Science, The University of Tokyo, Tokyo 108-8639, Japan e Department of Microbiology and Immunology, School of Medicine, Keio University, Tokyo 160-8582, Japan f Department of Parasitology, Institute of Tropical Medicine, Nagasaki University, Nagasaki 852-8523, Japan |
| 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. |
| Keywords: | IL-23 Interleukin-23 IL-17 Interleukin-17 RBC red blood cell Th T helper cells NK cells natural killer cells Treg regulatory T cell |
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