Time to activin on pathogenic T cells.
作者信息
Ebering Anna, Waisman Ari
机构信息
Institute for Molecular Medicine, University Medical Center, Johannes Gutenberg University Mainz, Mainz 55131, Germany.
Institute for Molecular Medicine, University Medical Center, Johannes Gutenberg University Mainz, Mainz 55131, Germany
出版信息
Proc Natl Acad Sci U S A. 2020 Jun 9;117(23):12513-12514. doi: 10.1073/pnas.2008491117. Epub 2020 May 22.
Abstract
摘要
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本文引用的文献
1
Activin-A limits Th17 pathogenicity and autoimmune neuroinflammation via CD39 and CD73 ectonucleotidases and Hif1-α-dependent pathways.激活素 A 通过 CD39 和 CD73 核苷酸酶以及 Hif1-α 依赖性途径限制 Th17 致病性和自身免疫性神经炎症。
Proc Natl Acad Sci U S A. 2020 Jun 2;117(22):12269-12280. doi: 10.1073/pnas.1918196117. Epub 2020 May 14.
2
Th17 cells increase in RRMS as well as in SPMS, whereas various other phenotypes of Th17 increase in RRMS only.Th17细胞在复发缓解型多发性硬化症（RRMS）以及继发进展型多发性硬化症（SPMS）中均有所增加，而Th17的其他多种表型仅在RRMS中增加。
Mult Scler J Exp Transl Clin. 2020 Jan 28;6(1):2055217319899695. doi: 10.1177/2055217319899695. eCollection 2020 Jan-Mar.
3
Unraveling the T-B tangle in anti-CD20 multiple sclerosis therapy.解析抗CD20治疗多发性硬化症中的T细胞与B细胞纠葛
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Pathogenic T cell cytokines in multiple sclerosis.多发性硬化症中的致病性 T 细胞细胞因子。
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