There are a broad range of disease-modifying therapies (DMTs) available in relapsing-remitting multiple sclerosis (RRMS), but limited biomarkers exist to personalise DMT choice. All DMTs, including monoclonal antibodies such as rituximab and ocrelizumab, are effective in preventing relapses and preserving neurological function in MS. However, each agent harbours its own risk of therapeutic failure or adverse events. Pharmacogenetics, the study of the effects of genetic variation on therapeutic response or adverse events, could improve the precision of DMT selection. Pharmacogenetic studies of rituximab in MS patients are lacking, but pharmacogenetic markers in other rituximab-treated autoimmune conditions have been identified. This review will outline the wider implications of pharmacogenetics and the mechanisms of anti-CD20 agents in MS. We explore the non-MS rituximab literature to characterise pharmacogenetic variants that could be of prognostic relevance in those receiving rituximab, ocrelizumab or other monoclonal antibodies for MS.

对于复发缓解型多发性硬化症 (RRMS)，有多种疾病缓解疗法 (DMT)，但用于个性化 DMT 选择的生物标志物有限。所有 DMT，包括单克隆抗体，如利妥昔单抗和奥瑞珠单抗，都能有效预防多发性硬化症复发并保留神经功能。然而，每种药物都有其自身的治疗失败或不良事件的风险。药物遗传学是研究遗传变异对治疗反应或不良事件影响的学科，可以提高 DMT 选择的精确度。缺乏多发性硬化症患者中利妥昔单抗的药物遗传学研究，但已鉴定出其他利妥昔单抗治疗的自身免疫性疾病的药物遗传学标志物。本综述将概述药物遗传学和抗 CD20 药物在多发性硬化症中的作用机制的更广泛影响。我们探索了非 MS 利妥昔单抗文献，以表征药物遗传学变异，这些变异可能与接受利妥昔单抗、ocrelizumab 或其他 MS 单克隆抗体治疗的患者的预后相关。