Volume 12, Issue 3 pp. 148-149
NEW DEVELOPMENTS IN NEUROIMMUNOLOGY

Interleukin-19 ameliorates experimental autoimmune encephalitis

Hideyuki Takeuchi

Corresponding Author

Hideyuki Takeuchi

Department of Neuroimmunology, Research Institute of Environmental Medicine, Nagoya University, Nagoya, Japan

Department of Neurology and Stroke Medicine, Yokohama City University Graduate School of Medicine, Yokohama, Japan

Correspondence: Hideyuki Takeuchi MD, PhD, Department of Neurology and Stroke Medicine, Yokohama City University Graduate School of Medicine. Fukuura 3-9, Kanazawa-ku, Yokohama 236-0004, Japan.

Email: [email protected]

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Hiroshi Horiuchi

Hiroshi Horiuchi

Department of Neuroimmunology, Research Institute of Environmental Medicine, Nagoya University, Nagoya, Japan

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Bijay Parajuli

Bijay Parajuli

Department of Neuroimmunology, Research Institute of Environmental Medicine, Nagoya University, Nagoya, Japan

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Hiroyasu Komiya

Hiroyasu Komiya

Department of Neurology and Stroke Medicine, Yokohama City University Graduate School of Medicine, Yokohama, Japan

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Fumiaki Tanaka

Fumiaki Tanaka

Department of Neurology and Stroke Medicine, Yokohama City University Graduate School of Medicine, Yokohama, Japan

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Akio Suzumura

Akio Suzumura

Department of Neuroimmunology, Research Institute of Environmental Medicine, Nagoya University, Nagoya, Japan

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First published: 29 March 2021

Graphical Abstract

Interleukin-19 serves as a negative feedback regulator to limit the pro-inflammatory response of macrophages and microglia in autocrine/paracrine manners. Interleukin-19 suppresses microglia/macrophage antigen presentation, T helper 17 cell expansion and subsequent inflammation in the central nervous system, resulting in improvement in experimental autoimmune encephalomyelitis.

Conflict of interest

The authors declare no conflict of interest.

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