Dimethyl fumarate suppresses Theiler’s murine encephalomyelitis virus-induced demyelinating disease by modifying the Nrf2-Keap1 pathway | Zendy

Kunitoshi Kobayashi | Zendy; Hiroki Tomiki | Zendy; Yuji Inaba | Zendy; Motoki Ichikawa | Zendy; ByungSoo Kim | Zendy; Chang-Sung Koh | Zendy

Open Access

Dimethyl fumarate suppresses Theiler’s murine encephalomyelitis virus-induced demyelinating disease by modifying the Nrf2-Keap1 pathway

Author(s) -

Kunitoshi Kobayashi,

Hiroki Tomiki,

Yuji Inaba,

Motoki Ichikawa,

ByungSoo Kim,

Chang-Sung Koh

Publication year - 2015

Publication title -

international immunology

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.86

H-Index - 134

eISSN - 1460-2377

pISSN - 0953-8178

DOI - 10.1093/intimm/dxv006

Subject(s) - demyelinating disease , dimethyl fumarate , virology , encephalomyelitis , keap1 , virus , chemistry , immunology , multiple sclerosis , medicine , biochemistry , gene , transcription factor

Dimethyl fumarate (DMF) is a modifier of the nuclear factor (erythroid-derived 2)-2 (Nrf2)-kelch-like ECH-associated protein 1 (Keap1) pathway. DMF treatment in the effector phase significantly suppressed the development of Theiler's murine encephalomyelitis virus-induced demyelinating disease (TMEV-IDD) both clinically and histologically. DMF treatment leads to an enhanced Nrf2 antioxidant response in TMEV-IDD mice. DMF treatment in the effector phase significantly suppressed the level of IL-17A mRNA. DMF is known to inhibit differentiation of T helper 17 (Th17) cells via suppressing NF-κB. Taken together, our data suggest that DMF treatment in the effector phase may suppress TMEV-IDD not only via enhancing the antioxidant response but also via suppressing IL-17A.

The content you want is available to Zendy users.

Already have an account? Click here to sign in.

Having issues? You can contact us here

Accelerating Research