IL-6-deficient mice are resistant to the induction of experimental autoimmune encephalomyelitis provoked by myelin oligodendrocyte glycoprotein

Yoshinobu Okuda, Saburo Sakoda, Claude C A Bernard, Harutoshi Fujimura, Yukihiko Saeki, Tadamitsu Kishimoto, Takehiko Yanagihara

Research output: Contribution to journalArticleResearchpeer-review

Abstract

The role of IL-6 in experimental autoimmune encephalomyelitis (EAE) provoked by myelin oligodendrocyte glycoprotein (MOG) was investigated using IL-6-deficient mice. We show here that IL-6-deficient mice were resistant to the MOG-induced EAE as compared to wild-type mice (one out of 18 versus 17 out of 20). The delayed-type hypersensitivity response, lymphocyte proliferation response and antibody reactivity to MOG in IL-6-deficient mice were significantly lower than those in wild-type mice. Furthermore, the histological examination revealed that no infiltration of inflammatory cells was observed in the central nervous system of IL-6-deficient mice. These results indicate that IL-6 may play a crucial role in the induction phase of EAE. Given the potential relevance of this animal model for multiple sclerosis (MS), it is possible that anti-IL-6 therapy may be useful in the prevention of relapses of MS.

Original languageEnglish
Pages (from-to)703-708
Number of pages6
JournalInternational Immunology
Volume10
Issue number5
DOIs
Publication statusPublished - 1998
Externally publishedYes

Keywords

  • Autoimmunity
  • Cytokines
  • Knockout mouse
  • Neuroimmunology

Cite this

Okuda, Yoshinobu ; Sakoda, Saburo ; Bernard, Claude C A ; Fujimura, Harutoshi ; Saeki, Yukihiko ; Kishimoto, Tadamitsu ; Yanagihara, Takehiko. / IL-6-deficient mice are resistant to the induction of experimental autoimmune encephalomyelitis provoked by myelin oligodendrocyte glycoprotein. In: International Immunology. 1998 ; Vol. 10, No. 5. pp. 703-708.
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abstract = "The role of IL-6 in experimental autoimmune encephalomyelitis (EAE) provoked by myelin oligodendrocyte glycoprotein (MOG) was investigated using IL-6-deficient mice. We show here that IL-6-deficient mice were resistant to the MOG-induced EAE as compared to wild-type mice (one out of 18 versus 17 out of 20). The delayed-type hypersensitivity response, lymphocyte proliferation response and antibody reactivity to MOG in IL-6-deficient mice were significantly lower than those in wild-type mice. Furthermore, the histological examination revealed that no infiltration of inflammatory cells was observed in the central nervous system of IL-6-deficient mice. These results indicate that IL-6 may play a crucial role in the induction phase of EAE. Given the potential relevance of this animal model for multiple sclerosis (MS), it is possible that anti-IL-6 therapy may be useful in the prevention of relapses of MS.",
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IL-6-deficient mice are resistant to the induction of experimental autoimmune encephalomyelitis provoked by myelin oligodendrocyte glycoprotein. / Okuda, Yoshinobu; Sakoda, Saburo; Bernard, Claude C A; Fujimura, Harutoshi; Saeki, Yukihiko; Kishimoto, Tadamitsu; Yanagihara, Takehiko.

In: International Immunology, Vol. 10, No. 5, 1998, p. 703-708.

Research output: Contribution to journalArticleResearchpeer-review

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AU - Okuda, Yoshinobu

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AU - Yanagihara, Takehiko

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