甘露糖结合凝集素途径不参与重症肌无力的发病机制。
Mannose-binding lectin pathway is not involved in myasthenia gravis pathogenesis.
作者信息
Li Jing, Qi Huibin, Tüzün Erdem, Allman Windy, Yilmaz Vuslat, Saini Shamsher S, Deymeer Feza, Saruhan-Direskeneli Güher, Christadoss Premkumar
机构信息
Department of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX, 77555-1070, USA.
出版信息
J Neuroimmunol. 2009 Mar 31;208(1-2):40-5. doi: 10.1016/j.jneuroim.2008.12.013. Epub 2009 Feb 3.
Classical complement pathway factor, C4 is required for experimental autoimmune myasthenia gravis (EAMG) pathogenesis. C4 is also a central component of the mannose binding lectin (MBL) pathway suggesting that this pathway might also be involved in MG pathogenesis. However, MBL gene deficient mice displayed intact anti-acetylcholine receptor (AChR)-immune response and neuromuscular junction (NMJ) IgG and complement accumulation following AChR-immunization. Moreover, no significant difference was observed between the serum MBL levels of 77 anti-AChR antibody positive generalized MG patients and 105 healthy controls. Therefore, MBL pathway does not play a role in EAMG/MG pathogenesis.
经典补体途径因子C4是实验性自身免疫性重症肌无力（EAMG）发病机制所必需的。C4也是甘露糖结合凝集素（MBL）途径的核心成分，这表明该途径可能也参与了重症肌无力的发病机制。然而，MBL基因缺陷小鼠在接受乙酰胆碱受体（AChR）免疫后，表现出完整的抗AChR免疫反应以及神经肌肉接头（NMJ）处IgG和补体的积累。此外，在77例抗AChR抗体阳性的全身型重症肌无力患者和105名健康对照者的血清MBL水平之间未观察到显著差异。因此，MBL途径在EAMG/重症肌无力的发病机制中不起作用。
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