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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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|February 14, 2024
PubMed
Summary
This summary is machine-generated.

Complement activation in the cerebrospinal fluid (CSF) is elevated in multiple sclerosis (MS) and clinically isolated syndrome (CIS), particularly with intrathecal IgM synthesis. This activation correlates with increased disease severity and progression, suggesting complement inhibition as a therapeutic target.

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Area of Science:

  • Neuroimmunology
  • Complement System Biology
  • Neurological Disorders

Background:

  • Histopathology reveals immunoglobulin (Ig) deposition and complement activation contribute to CNS damage in multiple sclerosis (MS).
  • Intrathecal IgM synthesis is linked to higher MS disease activity and severity.
  • IgM is the most potent immunoglobulin activator of the complement system.

Purpose of the Study:

  • To investigate elevated complement components (CCs) and complement activation products (CAPs) in individuals with MS.
  • To determine if CCs and CAPs are particularly increased in those with intrathecal IgM synthesis.
  • To assess the association between CC/CAP levels and MS disease severity and progression.

Main Methods:

  • Quantified CC and CAP levels in plasma and CSF of patients with clinically isolated syndrome (CIS), MS, inflammatory neurologic diseases, and controls.
  • Followed CIS/MS patients for a median of 6.3 years in the Swiss MS cohort study.
  • Utilized linear regression to analyze associations between CC/CAP levels, intrathecal Ig synthesis, EDSS, MSSS, and NfL, adjusting for covariates.

Main Results:

  • CSF levels of C3a, C4a, Ba, and Bb were elevated in CIS/MS patients, most notably with intrathecal IgM production.
  • Increased CSF C3a and C4a in CIS correlated with higher EDSS scores.
  • Elevated CSF C3a, C4a, Ba, and Bb in CIS/MS were associated with increased MS Severity Score (MSSS) and CSF neurofilament light chain (NfL) levels.

Conclusions:

  • Complement activation via classical and alternative pathways is increased within the CNS in CIS/MS, especially with intrathecal IgM production.
  • Elevated CSF complement activation correlates with disease severity (EDSS, MSSS) and progression markers (NfL).
  • Targeting complement inhibition may be a viable therapeutic strategy to reduce MS pathology and disease progression.