T cell metabolism connects complement and autoimmune regulation
T cell metabolism connects complement and autoimmune regulation
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T 细胞代谢连接补体和自身免疫调节
DOI：
10.1038/s41584-018-0027-3
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发表时间：
2018
影响因子：
33.7
通讯作者：
J. McHugh
中科院分区：
文献类型：
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作者：
J. McHugh
根据发表在《科学》杂志上的新研究，C1 q作为CD 8 + T细胞的代谢调节剂发挥作用，以抑制对自身抗原的反应并限制自身免疫。“在这项研究中，提供了关于为什么C1 q缺乏而不是C3缺乏与系统性红斑狼疮（SLE）的发展相关的见解，”没有参与这项研究的补体专家Leendert Trouw报告说。包括“废物处理”理论，即C1 q缺乏导致凋亡细胞的清除不足，因此增加了对自身抗原的暴露，导致自身免疫。然而，缺乏C3-缺陷和SLE发展之间的关联，以及其他冗余清除途径的存在，表明其他机制参与。
C1q functions as a metabolic regulator of CD8+ T cells to restrain responses to self-antigens and limit autoimmunity, according to new research published in Science.“In this study, insight is provided as to why C1q deficiency and not C3 deficiency is associated with the development of systemic lupus erythematosus (SLE),” reports Leendert Trouw, a complement expert who was not involved in the study.A number of theories exist to explain the association between C1q deficiency and SLE development, including the ‘waste-disposal’theory that C1q deficiency leads to inadequate clearance of apoptotic cells, and hence increased exposure to self-antigens, resulting in autoimmunity. However, the lack of an association between C3-deficiency and SLE development, and the existence of other redundant clearance pathways, indicates that other mechanisms are involved.