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

Hidekazu Ishida1, Chikako Matsuzaki-Moriya, Takashi Imai

  • 1Department of Microbiology and Immunology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.

Biochemical and Biophysical Research Communications
|November 2, 2010
PubMed

Insights

Interleukin-23 (IL-23) and Interleukin-17 (IL-17) do not appear to play a role in the development of experimental cerebral malaria (ECM). Studies in knockout and wild-type mice indicate these cytokines are not critical for ECM onset.

Area of Science:

  • Immunology
  • Infectious Diseases
  • Neuroscience

Background:

  • Cerebral malaria (CM) is a severe Plasmodium infection complication.
  • Inappropriate immune responses are implicated in CM pathogenesis, but mechanisms are unclear.
  • Interleukin-23 (IL-23) and Interleukin-17 (IL-17) are key in autoimmunity and inflammation.

Purpose of the Study:

  • To investigate the role of IL-23 and IL-17 in experimental cerebral malaria (ECM).

Main Methods:

  • Used Plasmodium berghei ANKA infection in C57BL/6 mice.
  • Utilized IL-23 deficient mice and IL-17 deficient mice.
  • Compared outcomes with wild-type (WT) mice.

Main Results:

  • Both IL-23 deficient and WT mice developed ECM.
  • IL-17 deficient mice also developed ECM.
  • Increased IL-17 producing cells (non-Th17) were observed in WT mice with ECM.

Conclusions:

  • IL-23 is not involved in the development of experimental cerebral malaria.
  • IL-17 is not involved in the development of experimental cerebral malaria.

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