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J Thromb Thrombolysis. 2020 Feb;49(2):228-234. doi: 10.1007/s11239-019-01970-2.
3
Myeloid cell-synthesized coagulation factor X dampens antitumor immunity.髓系细胞合成的凝血因子 X 抑制抗肿瘤免疫。
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蛋白 C 受体介导的脂质呈递将凝血与自身免疫联系起来。

Lipid presentation by the protein C receptor links coagulation with autoimmunity.

机构信息

Center for Thrombosis and Hemostasis, Johannes Gutenberg University Medical Center, 55131 Mainz, Germany.

Institute of Clinical Chemistry and Laboratory Medicine, Johannes Gutenberg University Medical Center, 55131 Mainz, Germany.

出版信息

Science. 2021 Mar 12;371(6534). doi: 10.1126/science.abc0956.

DOI:10.1126/science.abc0956
PMID:33707237
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9014225/
Abstract

Antiphospholipid antibodies (aPLs) cause severe autoimmune disease characterized by vascular pathologies and pregnancy complications. Here, we identify endosomal lysobisphosphatidic acid (LBPA) presented by the CD1d-like endothelial protein C receptor (EPCR) as a pathogenic cell surface antigen recognized by aPLs for induction of thrombosis and endosomal inflammatory signaling. The engagement of aPLs with EPCR-LBPA expressed on innate immune cells sustains interferon- and toll-like receptor 7-dependent B1a cell expansion and autoantibody production. Specific pharmacological interruption of EPCR-LBPA signaling attenuates major aPL-elicited pathologies and the development of autoimmunity in a mouse model of systemic lupus erythematosus. Thus, aPLs recognize a single cell surface lipid-protein receptor complex to perpetuate a self-amplifying autoimmune signaling loop dependent on the cooperation with the innate immune complement and coagulation pathways.

摘要

抗磷脂抗体 (aPL) 可导致严重的自身免疫性疾病，其特征为血管病变和妊娠并发症。在此，我们发现，内体溶血磷脂酰基酸 (LBPA) 通过 CD1d 样内皮蛋白 C 受体 (EPCR) 呈现，作为 aPL 识别的致病性细胞表面抗原，从而引发血栓形成和内体炎症信号转导。aPLs 与先天免疫细胞上表达的 EPCR-LBPA 的结合，维持了干扰素和 Toll 样受体 7 依赖性 B1a 细胞的扩增和自身抗体的产生。EPCR-LBPA 信号的特异性药理学阻断可减轻主要的 aPL 诱发的病变，并在系统性红斑狼疮的小鼠模型中发展自身免疫。因此，aPL 识别单一的细胞表面脂质-蛋白受体复合物，以维持自我放大的自身免疫信号循环，该循环依赖于与先天免疫补体和凝血途径的合作。