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Memory B Cells are Major Targets for Effective Immunotherapy in Relapsing Multiple Sclerosis.

Abstract：

:Although multiple sclerosis (MS) is considered to be a CD4, Th17-mediated autoimmune disease, supportive evidence is perhaps circumstantial, often based on animal studies, and is questioned by the perceived failure of CD4-depleting antibodies to control relapsing MS. Therefore, it was interestingly to find that current MS-treatments, believed to act via T cell inhibition, including: beta-interferons, glatiramer acetate, cytostatic agents, dimethyl fumarate, fingolimod, cladribine, daclizumab, rituximab/ocrelizumab physically, or functionally in the case of natalizumab, also depleted CD19+, CD27+ memory B cells. This depletion was substantial and long-term following CD52 and CD20-depletion, and both also induced long-term inhibition of MS with few treatment cycles, indicating induction-therapy activity. Importantly, memory B cells were augmented by B cell activating factor (atacicept) and tumor necrosis factor (infliximab) blockade that are known to worsen MS. This creates a unifying concept centered on memory B cells that is consistent with therapeutic, histopathological and etiological aspects of MS.

journal_name

EBioMedicine

journal_title

EBioMedicine

authors

Baker D,Marta M,Pryce G,Giovannoni G,Schmierer K

doi

10.1016/j.ebiom.2017.01.042

subject

Has Abstract

pub_date

2017-02-01 00:00:00

pages

41-50

issn

2352-3964

pii

S2352-3964(17)30045-2

journal_volume

16

pub_type

杂志文章,评审

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