Stergiou Christos, Williams Rhys, Fleming Jennifer R, Zouvelou Vasiliki, Ninou Elpinickie, Andreetta Francesca, Rinaldi Elena, Simoncini Ornella, Mantegazza Renato, Bogomolovas Julius, Tzartos John, Labeit Siegfried, Mayans Olga, Tzartos Socrates
Tzartos NeuroDiagnostics, 115 23 Athens, Greece.
Department of Biology, University of Konstanz, 78457 Konstanz, Germany.
Biomedicines. 2023 Feb 3;11(2):449. doi: 10.3390/biomedicines11020449.
Myasthenia gravis (MG) is an autoimmune disease caused by antibodies targeting the neuromuscular junction (NJ) of skeletal muscles. The major MG autoantigen is nicotinic acetylcholine receptor. Other autoantigens at the NJ include MuSK, LRP4 and agrin. Autoantibodies to the intra-sarcomeric striated muscle-specific gigantic protein titin, although not directed to the NJ, are invaluable biomarkers for thymoma and MG disease severity. Thymus and thymoma are critical in MG mechanisms and management. Titin autoantibodies bind to a 30 KDa titin segment, the main immunogenic region (MIR), consisting of an Ig-FnIII-FnIII 3-domain tandem, termed I109-I111. In this work, we further resolved the localization of titin epitope(s) to facilitate the development of more specific anti-titin diagnostics. For this, we expressed protein samples corresponding to 8 MIR and non-MIR titin fragments and tested 77 anti-titin sera for antibody binding using ELISA, competition experiments and Western blots. All anti-MIR antibodies were bound exclusively to the central MIR domain, I110, and to its containing titin segments. Most antibodies were bound also to SDS-denatured I110 on Western blots, suggesting that their epitope(s) are non-conformational. No significant difference was observed between thymoma and non-thymoma patients or between early- and late-onset MG. In addition, atomic 3D-structures of the MIR and its subcomponents were elucidated using X-ray crystallography. These immunological and structural data will allow further studies into the atomic determinants underlying titin-based autoimmunity, improved diagnostics and how to eventually treat titin autoimmunity associated co-morbidities.
重症肌无力(MG)是一种自身免疫性疾病,由靶向骨骼肌神经肌肉接头(NJ)的抗体引起。MG的主要自身抗原是烟碱型乙酰胆碱受体。NJ处的其他自身抗原包括肌肉特异性激酶(MuSK)、低密度脂蛋白受体相关蛋白4(LRP4)和聚集蛋白。针对肌节内横纹肌特异性巨大蛋白肌联蛋白的自身抗体,虽然不针对NJ,但对于胸腺瘤和MG疾病严重程度而言是非常重要的生物标志物。胸腺和胸腺瘤在MG的发病机制及治疗中起着关键作用。肌联蛋白自身抗体与一个30 kDa的肌联蛋白片段结合,该片段是主要免疫原性区域(MIR),由一个免疫球蛋白-纤连蛋白III-纤连蛋白III 3结构域串联组成,称为I109-I111。在这项研究中,我们进一步确定了肌联蛋白表位的定位,以促进更具特异性的抗肌联蛋白诊断方法的开发。为此,我们表达了对应于8个MIR和非MIR肌联蛋白片段的蛋白质样品,并使用酶联免疫吸附测定(ELISA)、竞争实验和蛋白质免疫印迹法检测了77份抗肌联蛋白血清的抗体结合情况。所有抗MIR抗体仅与中央MIR结构域I110及其包含的肌联蛋白片段结合。大多数抗体在蛋白质免疫印迹中也与十二烷基硫酸钠(SDS)变性的I110结合,这表明它们的表位是非构象性的。在胸腺瘤患者和非胸腺瘤患者之间,以及早发型和晚发型MG患者之间均未观察到显著差异。此外,利用X射线晶体学阐明了MIR及其亚组分的原子三维结构。这些免疫学和结构数据将有助于进一步研究基于肌联蛋白的自身免疫的原子决定因素、改进诊断方法以及最终如何治疗与肌联蛋白自身免疫相关的合并症。