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MINI REVIEW article
Front. Immunol.
Sec. Autoimmune and Autoinflammatory Disorders : Autoimmune Disorders
Volume 16 - 2025 | doi: 10.3389/fimmu.2025.1526317
The role of complement in the immunopathogenesis of acetylcholine receptor antibody-positive generalized myasthenia gravis: bystander or key player?
Provisionally accepted
Iliana Michailidou 1
Anastasia Patsiarika 2
Evangelia Kesidou 1
Marina Kleopatra Boziki 1,3
Dimitrios Parissis 3
Christos Bakirtzis 3
Elisabeth Chroni 4
Nikolaos Grigoriadis 1,3*- 1 Laboratory of Experimental Neurology and Neuroimmunology, AHEPA University Hospital, Aristotle University of Thessaloniki, Greece, Thessaloniki, Greece
- 2 AstraZeneca Rare Disease, Athens, Greece, Athens, Greece
- 3 Dept. Neurology II, AHEPA University Hospital, Aristotle University of Thessaloniki, Greece, Thessaloniki, Greece
- 4 Dept. Neurology, Medical School, University of Patras, Greece, Patras, Greece
The complement system is a key component of the innate immune system. In anti-acetylcholine receptor (AChR) antibody positive (Ab+) generalized myasthenia gravis (MG), activated complement has long been considered a principal mechanism driving pathology. Determining the roles of complement in the pathogenesis of AChR-Ab+ generalized MG has become very important in recent years since anti-complement drugs have been approved for clinical use or are undergoing phase II/III clinical trials. The purpose of this review is to discuss recent and previous findings on the contribution of complement to AChR-Ab+ MG pathology by binding to pathogenic antibodies and beyond the antibody-mediated paradigm of classical pathway activation.
Keywords: Myasthenia Gravis, complement system, Anti-acetylcholine receptor antibodies, Membrane attack complex, therapy
Received: 11 Nov 2024; Accepted: 24 Mar 2025.
Copyright: © 2025 Michailidou, Patsiarika, Kesidou, Boziki, Parissis, Bakirtzis, Chroni and Grigoriadis. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence:
Nikolaos Grigoriadis, Laboratory of Experimental Neurology and Neuroimmunology, AHEPA University Hospital, Aristotle University of Thessaloniki, Greece, Thessaloniki, Greece
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