多发性硬化症的B细胞靶向治疗策略：从非细胞疗法到CAR工程化细胞疗法
B-cell targeting strategies for the treatment of multiple sclerosis: from non-cellular therapies to CAR-engineered cell therapies
越来越多证据显示B细胞谱系在多发性硬化症（一种中枢神经系统自身免疫病）发病中居核心地位，抗CD20单克隆抗体的成功更确立了B细胞耗竭疗法的地位。但现有疗法仍不能完全控制中枢神经系统内的局部免疫反应，且清除范围过宽。这篇综述梳理了已确立的非细胞策略（单克隆抗体、布鲁顿酪氨酸激酶抑制剂、B细胞活化因子抑制剂），并重点讨论新兴的嵌合抗原受体（CAR）工程化细胞疗法。作者认为CAR细胞疗法有望实现更彻底、更持久的致病B细胞清除，包括中枢神经系统内驻留的B细胞亚群，是值得期待的前沿方向，但仍面临挑战。
为什么推荐给您：系统梳理B细胞靶向治疗包括CAR细胞疗法这一新兴方向，属值得关注，但本身为综述。
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摘要Abstract
BACKGROUND: Accumulating evidence indicates that B-cell lineages play a central role in the pathogenesis of multiple sclerosis (MS). This understanding has reshaped the therapeutic landscape of MS, particularly following the success of anti-CD20 monoclonal antibodies (mAbs), which have become a cornerstone of MS treatment. Despite their efficacy in reducing relapse rates and slowing disability accumulation, current B-cell-depleting therapies have important limitations, including incomplete control of compartmentalized immune responses within the central nervous system (CNS).
METHODS: This review summarizes the progress and limitations of current and emerging B-cell-targeting strategies for MS. We discuss established non-cellular approaches, including monoclonal antibodies, Bruton's tyrosine kinase (BTK) inhibitors, and B-cell activating factor (BAFF) inhibitors, and examine the rationale, potential advantages, and challenges of emerging chimeric antigen receptor (CAR)-engineered cell therapies.
RESULTS: Anti-CD20 mAbs have demonstrated significant clinical efficacy; however, their limited CNS penetration and broad depletion of B-cell populations highlight the need for more targeted approaches. BTK inhibitors represent an emerging strategy to modulate B-cell and myeloid-cell signaling, while BAFF-targeting therapies have provided important insights into the complex role of B-cell survival pathways in MS. CAR-engineered cell therapies have emerged as a promising cellular approach capable of inducing profound and potentially durable depletion of pathogenic B-cell populations, including CNS-resident B-cell subsets.
CONCLUSIONS: B-cell-targeting therapies continue to expand the therapeutic landscape of MS. Although current non-cellular approaches have improved disease control, their limitations emphasize the need for next-generation strategies. CAR-engineered cell therapies represent a promising frontier with the potential to achieve more sustained immune modulation and address some unmet therapeutic challenges in MS.