The Walter and Eliza Hall Institute of Medical Research, Parkville, VIC, 3052, Australia; The Department of Medical Biology, University of Melbourne, Parkville, VIC, 3010, Australia.
The Walter and Eliza Hall Institute of Medical Research, Parkville, VIC, 3052, Australia; The Department of Medical Biology, University of Melbourne, Parkville, VIC, 3010, Australia.
Curr Opin Immunol. 2021 Feb;68:83-97. doi: 10.1016/j.coi.2020.09.008. Epub 2020 Nov 4.
The necroptotic cell death pathway has received significant attention for its ability to trigger inflammatory responses and its potential involvement in related conditions. Recent insights into the essential membrane damaging necroptotic pseudokinase effector, Mixed lineage kinase domain like (MLKL), have revealed a number of diverse MLKL functions that contribute to the inflammatory nature of necroptosis. Here we review distinct MLKL signalling roles and document the immunogenic molecules released by necroptosis. We discuss specific in vivo MLKL-driven responses, the activation of inflammasome complexes and innate lymphoid cells, which have been documented to drive disease. Finally, we list necroptotic competent cell types and their involvement in MLKL-driven cell death-associated and inflammatory-associated conditions.
细胞坏死性细胞死亡途径因其能够引发炎症反应及其在相关疾病中的潜在作用而受到广泛关注。最近对关键的膜损伤性坏死性拟激酶效应物混合谱系激酶结构域样（MLKL）的深入了解揭示了许多不同的 MLKL 功能，这些功能有助于坏死性细胞死亡的炎症性质。在这里，我们回顾了不同的 MLKL 信号作用，并记录了坏死性细胞死亡释放的免疫原性分子。我们讨论了特定的体内 MLKL 驱动的反应，即炎症小体复合物和固有淋巴细胞的激活，这些反应已被证明可导致疾病。最后，我们列出了具有坏死能力的细胞类型及其在 MLKL 驱动的细胞死亡相关和炎症相关疾病中的作用。
