Currently, disease-modifying therapies for multiple sclerosis (MS) use 4 mechanisms of action: immune modulation, suppressing immune cell proliferation, inhibiting immune cell migration, or cellular depletion. Over the last decades, the repertoire substantially increased because of the conceptual progress that not only T cells but also B cells play an important pathogenic role in MS, fostered by the empirical success of B cell-depleting antibodies against the surface molecule CD20. Notwithstanding this advance, a continuous absence of B cells may harbor safety risks, such as a decline in the endogenous production of immunoglobulins. Accordingly, novel B cell-directed MS therapies are in development, such as inhibitors targeting Bruton tyrosine kinase (BTK).

中文翻译：

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用 Bruton 酪氨酸激酶抑制剂靶向多发性硬化症中的 B 细胞和小胶质细胞：综述。

目前，多发性硬化症 (MS) 的疾病缓解疗法使用 4 种作用机制：免疫调节、抑制免疫细胞增殖、抑制免疫细胞迁移或细胞耗竭。在过去的几十年里，由于不仅 T 细胞而且 B 细胞在 MS 中发挥重要致病作用的概念进展，由于针对表面分子 CD20 的 B 细胞耗竭抗体的经验成功促进了这一概念的进展，因此在过去的几十年中，曲目大大增加。尽管取得了这一进展，但持续缺乏 B 细胞可能会带来安全风险，例如内源性免疫球蛋白产量下降。因此，新的 B 细胞定向 MS 疗法正在开发中，例如针对布鲁顿酪氨酸激酶 (BTK) 的抑制剂。