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补充激活与多发性硬化症的疾病严重程度有关.

Johanna Oechtering1, Kerstin Stein1, Sabine A Schaedelin1

  • 1From the Department of Neurology (J.O., A.M.M., A.O., S. Meier, E.W., T.D., M.D.S., M.L., B.F.-B., C. Granziera, L.K., D.L., J.K.); Multiple Sclerosis Centre and Research Center for Clinical Neuroimmunology and Neuroscience (RC2NB) (J.O., S.A.S., A.M.M., A.O., S. Meier, E.W., T.D., P.B., M.D.S., M.L., B.F.-B., C. Granziera, L.K., D.L., J.K.), Departments of Biomedicine and Clinical Research, University Hospital and University of Basel, Switzerland; Department of Neurology with Institute of Translational Neurology (K.S., H.W., J.D.L.), University Hospital 4 Münster, Germany; Clinical Trial Unit (S.A.S., P.B.), Department of Clinical Research, University Hospital Basel, University of Basel, Basel, Switzerland; Octavebio Bioscience (F.Q.), Menlo Park, CA; Division of Medical Immunology (I.H.), Laboratory Medicine, University Hospital Basel, Switzerland; Medica Laboratory (A.R.), Zürich; Department of Neurology (L.A.), Cantonal Hospital, Aarau; Department of Neurology (S. Mueller), Cantonal Hospital St. Gallen; Department of Neurology (A.S.), Inselspital, Bern University Hospital and University of Bern; Department of Clinical Neurosciences (P.H.L., C.B.), Division of Neurology; Diagnostic Department (P.H.L.), Division of Laboratory Medicine; Department of Pathology and Immunology (P.H.L.), Faculty of Medicine, University of Geneva; Division of Neurology (C.P., R.A.D.P.), Department of Clinical Neurosciences, Lausanne University Hospital (CHUV) and University of Lausanne; Neurocentre of Southern Switzerland (C. Gobbi), Multiple Sclerosis Centre, Ospedale Civico; Faculty of Biomedical Sciences (C. Gobbi), Università della Svizzera Italiana (USI), Lugano, Switzerland; Translational Imaging in Neurology (ThINk) Basel (C. Granziera), Department of Biomedical Engineering, Faculty of Medicine, University Hospital Basel and University of Basel; and Division of Internal Medicine (M.T.), University Hospital Basel and Clinical Immunology, Department of Biomedicine, University of Basel, Basel, Switzerland.

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脑脊液 (CSF) 中的补充激活在多发性硬化症 (MS) 和临床隔离综合征 (CIS) 中升高,特别是在内IgM合成中. 这种激活与疾病严重程度和进展的增加相关,这表明补充抑制作为治疗点.

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科学领域:

  • 神经免疫学 神经免疫学
  • 补充系统生物学 补充系统生物学
  • 神经系统疾病 神经系统疾病

背景情况:

  • 组织病理学显示,免疫球蛋白 (Ig) 沉积和补体激活有助于在多发性硬化症 (MS) 中的中枢神经系统损伤.
  • 内IgM合成与更高的MS疾病活性和严重程度有关.
  • IgM 是补充系统中最强大的免疫球蛋白激活剂.

研究的目的:

  • 在MS患者中研究补充成分 (CCs) 和补充激活产品 (CAPs) 的升高.
  • 为了确定CCs和CAPs是否特别增加,在那些与内IgM合成.
  • 评估CC/CAP水平与MS疾病严重程度和进展之间的关联.

主要方法:

  • 临床隔离综合征 (CIS),多发性硬化症,炎症神经系统疾病和对照患者的血和脑脊髓液中的量化CC和CAP水平.
  • 在瑞士MS队列研究中,追踪CIS/MS患者的中位数为6.3年.
  • 使用线性回归来分析CC/CAP水平之间的关联,内Ig合成,EDSS,MSSS和NfL,调整共变量.

主要成果:

  • 脑液中C3a,C4a,Ba和Bb的水平在CIS/MS患者中升高,最显著的是内IgM的产生.
  • 在CIS中增加的CSF C3a和C4a与更高的EDSS分数相关.
  • 在CIS/MS中增加的CSF C3a,C4a,Ba和Bb与增加的MS严重性评分 (MSSS) 和CSF神经纤维光链 (NfL) 水平有关.

结论:

  • 在CIS/MS中,通过经典和替代途径在中枢神经系统内增加补充激活,特别是在内IgM产生时.
  • 增加的CSF补充激活与疾病严重程度 (EDSS,MSSS) 和进展标志物 (NfL) 相相关.
  • 向补充抑制可能是一个可行的治疗策略,以减少多发性硬化病理和疾病进展.