Department of Biomedicine, University Hospital Basel, Switzerland.
Mol Immunol. 2022 Nov;151:11-18. doi: 10.1016/j.molimm.2022.08.018. Epub 2022 Sep 2.
Myasthenia gravis is a neuromuscular disease associated with antibodies against components of the neuromuscular junction, most often against the acetylcholine receptor (AChR). Although several mechanisms have been postulated to explain how these autoantibodies can lead to the pathology of the disease, convincing evidence suggests that destruction of the receptor-bearing postsynaptic membrane by complement membrane attack complex is of central importance. In this review, evidence for the importance of complement, and possible relationships between autoantigen, autoantibodies, complement activation, and the destruction of the membrane are discussed. More recent insights from the results of the complement-inhibiting therapeutic antibody eculizumab are also described, and the mechanisms connecting antibody binding to complement activation are considered from a structural viewpoint.
重症肌无力是一种与神经肌肉接头成分抗体相关的神经肌肉疾病,最常见的是针对乙酰胆碱受体 (AChR)。尽管已经提出了几种机制来解释这些自身抗体如何导致疾病的病理学,但令人信服的证据表明,补体膜攻击复合物破坏带受体的突触后膜具有核心重要性。在这篇综述中,讨论了补体的重要性的证据,以及自身抗原、自身抗体、补体激活和膜破坏之间的可能关系。还描述了来自补体抑制治疗抗体依库珠单抗的结果的最新见解,并从结构角度考虑了抗体结合与补体激活之间的连接机制。