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CD20+ T cells as pathogenic players and therapeutic targets in MS.

Ann Neurol. 2021 Sep 29. doi: 10.1002/ana.26232. Epub ahead of print. PMID: 34585761.

Authors/Editors: Meinl E, Hohlfeld R.
Publication Date: 2021


Success of anti-CD20 therapy has placed B cells center stage, to an extent that T cells are becoming perceived as minor players in the pathogenesis of multiple sclerosis (MS). However, anti-CD20 therapy not only depletes CD20+ B cells, but also a very distinct subset of CD20+ T cells which has pro-inflammatory features.1-6 In this issue of the Annals of Neurology, Quendt et al show that different approved therapies affect this subset of T cells differently.5 They show that DMF reduces expression of chemokine receptors, such as CXCR3 as well as the cytokine-producing ability of CD20+ T cells. Fingolimod reduces these cells in the blood as part of its overall T-cell depleting effect. Natalizumab increases the level of circulating CD20+ T cells, in line with the concept that blocking α4 integrin prevents the exit of encephalitogenic T cells from blood. This confirms and extends previous observations describing effects of fingolimod, DMF, and natalizumab,2 as well as alemtuzumab4 on CD20+ T cells. Quendt et al further show that these CD20+ T cells produce increased amounts of the encephalitogenic cytokines GM-CSF, IFN-γ, IL-17, and TNF-α as well as the regulatory cytokines IL-4 and IL-10.5 This extends previous reports about the cytokine profile of CD20+ T cells2, 4 and their expression of the cytotoxic markers perforin and GzmB. 

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