CD98 is a potential target for ablating B cell clonal expansion and autoantibody in multiple sclerosis.

CD98 is a potential target for ablating B cell clonal expansion and autoantibody in multiple sclerosis.
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DOI:
10.1016/j.jneuroim.2014.06.015
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发表时间:
2014-09-15
影响因子:
3.3
通讯作者:
Cantor, Joseph M.
Cantor, Joseph M.
中科院分区:
医学4区
文献类型:
--
作者:
Cantor, Joseph M.

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目前针对多发性硬化症的B细胞定向疗法影响多种B细胞功能。CD98hc使B细胞克隆扩增和抗体产生。我探讨了自身抗体分泌相对于MS中其他B细胞功能的相对重要性,并将靶向CD98hc作为可能的治疗策略。我报告了B细胞中CD98hc功能的丧失在很大程度上阻止了自身抗体的产生,同时保留了抗原呈递和T细胞定向能力。B细胞中缺乏CD98hc的小鼠对EAE具有保护作用;重要的是,这可以用含有自身抗体的血浆来克服。因此,CD98hc阻断是通过抑制克隆扩增和自身抗体治疗多发性硬化症的可能途径。
Current B cell-directed therapies for multiple sclerosis impact multiple B cell functions. CD98hc enables B cell clonal expansion and antibody production. I probed the relative importance of autoantibody secretion vs. other B cell functions in MS and targeted CD98hc as a possible therapeutic strategy. I report that loss of CD98hc function in B cells largely prevents autoantibody production while preserving antigen-presenting and T cell-directing capacities. Mice lacking CD98hc in B cells are protected from EAE; importantly this is overcome with autoantibody-containing plasma. Thus CD98hc blockade is a possible avenue to treat MS by inhibiting clonal expansion and autoantibody.
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