伊塔康酸通过诱导 PD-L1 促进疟疾的发生。

Yukun Min, Luke A J O'Neill
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引用次数: 0

摘要

克雷布斯循环衍生的代谢物伊塔康酸已被证明具有免疫调节作用,可针对巨噬细胞的多个过程。1 查鲍迪疟原虫会诱导树突状细胞(DCs)中的衣康酸盐,导致程序性死亡配体 1(PD-L1)诱导。这抑制了 CD8+ T 细胞,而 CD8+ T 细胞是宿主防御疟疾的重要细胞,从而促进了寄生虫血症。
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Itaconate boosts malaria via induction of PD-L1.

The Krebs-cycle-derived metabolite itaconate has been shown to be immunomodulatory, targeting multiple processes in macrophages. Ramalho et al. reveal an additional role for itaconate in malaria.1Plasmodium Chabaudi induces itaconate in dendritic cells (DCs), leading to programmed death-ligand 1 (PD-L1) induction. This suppresses CD8+ T cells, important for host defense against malaria, thereby promoting parasitemia.

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