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Comment on "the pro-factor D cleaving activity of MASP-1/-3 is not required for alternative pathway function".

作者信息

Takahashi Minoru, Sekine Hideharu, Fujita Teizo

机构信息

Department of Immunology, Fukushima Medical University School of Medicine, Fukushima 960-1295, Japan

Department of Immunology, Fukushima Medical University School of Medicine, Fukushima 960-1295, Japan.

出版信息

J Immunol. 2014 Jun 15;192(12):5448-9. doi: 10.4049/jimmunol.1400766.

DOI:10.4049/jimmunol.1400766
PMID:24907377
Abstract
摘要

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The pro-factor D cleaving activity of MASP-1/-3 is not required for alternative pathway function.旁路途径功能并不需要MASP-1/-3的前因子D裂解活性。
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Quantification of the zymogenicity and the substrate-induced activity enhancement of complement factor D.补体因子 D 的酶原活力和底物诱导活性增强的定量分析。
Front Immunol. 2023 May 22;14:1197023. doi: 10.3389/fimmu.2023.1197023. eCollection 2023.
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Extensive Basal Level Activation of Complement Mannose-Binding Lectin-Associated Serine Protease-3: Kinetic Modeling of Lectin Pathway Activation Provides Possible Mechanism.补体甘露糖结合凝集素相关丝氨酸蛋白酶-3的广泛基础水平激活：凝集素途径激活的动力学模型提供了可能的机制。
Front Immunol. 2017 Dec 18;8:1821. doi: 10.3389/fimmu.2017.01821. eCollection 2017.
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Mannan-Binding Lectin-Associated Serine Protease 1/3 Cleavage of Pro-Factor D into Factor D In Vivo and Attenuation of Collagen Antibody-Induced Arthritis through Their Targeted Inhibition by RNA Interference-Mediated Gene Silencing.
甘露糖结合凝集素相关丝氨酸蛋白酶1/3在体内将前因子D裂解为因子D，并通过RNA干扰介导的基因沉默对其进行靶向抑制，从而减轻胶原抗体诱导的关节炎。
J Immunol. 2016 Nov 1;197(9):3680-3694. doi: 10.4049/jimmunol.1600719. Epub 2016 Oct 5.
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MASP-3 is the exclusive pro-factor D activator in resting blood: the lectin and the alternative complement pathways are fundamentally linked.MASP-3 是静息血液中唯一的因子 D 前体激活物：凝集素和替代补体途径从根本上是相关联的。
Sci Rep. 2016 Aug 18;6:31877. doi: 10.1038/srep31877.
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Novel MASP1 mutations are associated with an expanded phenotype in 3MC1 syndrome.新型MASP1突变与3MC1综合征的扩展表型相关。
Orphanet J Rare Dis. 2015 Sep 30;10:128. doi: 10.1186/s13023-015-0345-3.
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Essential role for the lectin pathway in collagen antibody-induced arthritis revealed through use of adenovirus programming complement inhibitor MAp44 expression.通过使用腺病毒编程补体抑制剂MAp44表达揭示凝集素途径在胶原抗体诱导的关节炎中的重要作用。
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