CD98 是多发性硬化症中 B 细胞克隆扩增和自身抗体的潜在靶点。
CD98 is a potential target for ablating B cell clonal expansion and autoantibody in multiple sclerosis.
机构信息
Department of Medicine, University of California San Diego, MC 0726, 9500 Gilman Drive, La Jolla, CA 92093-0726, United States.
出版信息
J Neuroimmunol. 2014 Sep 15;274(1-2):230-3. doi: 10.1016/j.jneuroim.2014.06.015. Epub 2014 Jun 26.
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 the 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.
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 可促进 B 细胞克隆扩增和抗体产生。我探究了自身抗体分泌与 MS 中其他 B 细胞功能的相对重要性，并将 CD98hc 作为一种可能的治疗策略。我报告说，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 细胞导向能力。缺乏 B 细胞中 CD98hc 的小鼠可免受 EAE 的侵害；重要的是，含有自身抗体的血浆可以克服这一点。因此，CD98hc 阻断可能是通过抑制克隆扩增和自身抗体来治疗多发性硬化症的一种途径。
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