Unexpected exacerbations following initiation of disease-modifying drugs in neuromyelitis optica spectrum disorder: Which factor is responsible, anti-aquaporin 4 antibodies, B cells, Th1 cells, Th2 cells, Th17 cells, or others?

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Unexpected exacerbations following initiation of disease-modifying drugs in neuromyelitis optica spectrum disorder: Which factor is responsible, anti-aquaporin 4 antibodies, B cells, Th1 cells, Th2 cells, Th17 cells, or others? is …
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scholarly articleQ13442814

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P356DOI10.1177/1352458517703803
P698PubMed publication ID28391741

P2093author name stringJun-Ichi Kira
P2860cites workPlacebo-controlled phase 3 study of oral BG-12 for relapsing multiple sclerosisQ28275399
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Fumaric acid esters exert neuroprotective effects in neuroinflammation via activation of the Nrf2 antioxidant pathway.Q34627230
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Fingolimod (FTY720) therapy in Japanese patients with relapsing multiple sclerosis over 12 months: results of a phase 2 observational extensionQ37548575
Neuromyelitis optica: pathogenicity of patient immunoglobulin in vivo.Q39770767
Catastrophic relapses following initiation of dimethyl fumarate in two patients with neuromyelitis optica spectrum disorderQ47924759
Emerging tumefactive multiple sclerosis after switching therapy from natalizumab to fingolimodQ48319736
Tumefactive multiple sclerosis lesions under fingolimod treatmentQ48350609
P433issue9
P921main subjectneuromyelitis opticaQ611458
P304page(s)1300-1302
P577publication date2017-04-10
P1433published inMultiple Sclerosis JournalQ1952449
P1476titleUnexpected exacerbations following initiation of disease-modifying drugs in neuromyelitis optica spectrum disorder: Which factor is responsible, anti-aquaporin 4 antibodies, B cells, Th1 cells, Th2 cells, Th17 cells, or others?
P478volume23

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