Oxygenated phosphatidylethanolamine navigates phagocytosis of ferroptotic cells by interacting with TLR2

Luo, Xiang; Gong, Haibiao; Gao, Huaying; Wu, Yanping; Sun, Wanyang; Li, Zhengqiu; Wang, Guan; Liu, Bo; Liu, Liang; Kojima, Hiroshi; Duan, Wen-Jun; Li, Yi-Fang; He, Rong‐Rong

doi:10.1038/s41418-020-00719-2

Cited by 154 publications

(110 citation statements)

References 47 publications

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“…This finding reinforces the notion that nonapoptotic cell death, including ferroptosis, is more likely to cause inflammation than apoptosis. In contrast, ferroptotic cells can produce oxygenated phosphatidylethanolamines on the outer plasma membrane that can be recognized by TLR2 on macrophages, leading to the clearance of ferroptotic cells ( Luo et al, 2021 ).…”

Section: Ferroptosis In Immune Cellsmentioning

confidence: 99%

Ferroptosis in infection, inflammation, and immunity

Chen

Kang

Kroemer

et al. 2021

Journal of Experimental Medicine

447

231

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Ferroptosis is a type of regulated necrosis that is triggered by a combination of iron toxicity, lipid peroxidation, and plasma membrane damage. The upstream inducers of ferroptosis can be divided into two categories (biological versus chemical) and activate two major pathways (the extrinsic/transporter versus the intrinsic/enzymatic pathways). Excessive or deficient ferroptotic cell death is implicated in a growing list of physiological and pathophysiological processes, coupled to a dysregulated immune response. This review focuses on new discoveries related to how ferroptotic cells and their spilled contents shape innate and adaptive immunity in health and disease. Understanding the immunological characteristics and activity of ferroptotic death not only illuminates an intersection between cell death and immunity but may also lead to the development of novel treatment approaches for immunopathological diseases.

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Section: Ferroptosis In Immune Cellsmentioning

confidence: 99%

Ferroptosis in infection, inflammation, and immunity

Chen

Kang

Kroemer

et al. 2021

Journal of Experimental Medicine

447

231

View full text Add to dashboard Cite

show abstract

“…The lectin-like OxLDL receptor 1 (LOX-1) can mediate phagocytosis of aged and apoptotic cells, possibly by binding oxidised low-density lipoproteins (LDLs) on these cells ( 63 ). Oxidized phosphatidylethanolamine exposed on the surface of cells undergoing ferroptosis (an iron-dependent form of programmed cell death) triggers macrophage phagocytosis of these cells via the macrophage toll-like receptor 2 (TLR2) ( 65 ).…”

Section: The Phagocytic Codementioning

confidence: 99%

The Phagocytic Code Regulating Phagocytosis of Mammalian Cells

et al. 2021

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Mammalian phagocytes can phagocytose (i.e. eat) other mammalian cells in the body if they display certain signals, and this phagocytosis plays fundamental roles in development, cell turnover, tissue homeostasis and disease prevention. To phagocytose the correct cells, phagocytes must discriminate which cells to eat using a ‘phagocytic code’ - a set of over 50 known phagocytic signals determining whether a cell is eaten or not - comprising find-me signals, eat-me signals, don’t-eat-me signals and opsonins. Most opsonins require binding to eat-me signals – for example, the opsonins galectin-3, calreticulin and C1q bind asialoglycan eat-me signals on target cells - to induce phagocytosis. Some proteins act as ‘self-opsonins’, while others are ‘negative opsonins’ or ‘phagocyte suppressants’, inhibiting phagocytosis. We review known phagocytic signals here, both established and novel, and how they integrate to regulate phagocytosis of several mammalian targets - including excess cells in development, senescent and aged cells, infected cells, cancer cells, dead or dying cells, cell debris and neuronal synapses. Understanding the phagocytic code, and how it goes wrong, may enable novel therapies for multiple pathologies with too much or too little phagocytosis, such as: infectious disease, cancer, neurodegeneration, psychiatric disease, cardiovascular disease, ageing and auto-immune disease.

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“…Damage-associated molecular patterns (DAMPs), PGE2, and other substances released by ferroptotic cells can inhibit or activate immune cells 65 , although it remains unclear whether ferroptotic cells will release specific substances to regulate the immune system. Also, oxidized phospholipids on the cell membrane act as "eat me" signals 66 when ferroptosis sets off and recruits phagocytes. Since the EMT status of cells is highly sensitive to ferroptosis, the tumor microenvironment becomes the key to their migration success rate.…”

Section: Ideas For the Development Of Nanomaterials To Target Ferroptosismentioning

confidence: 99%

Targeting ferroptosis-based cancer therapy using nanomaterials: strategies and applications

et al. 2021

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As an iron-dependent mode of programmed cell death induced by lipid peroxidation, ferroptosis plays an important role in cancer therapy. The metabolic reprogramming in tumor microenvironment allows the possibility of targeting ferroptosis in cancer treatment. Recent studies reveal that nanomaterials targeting ferroptosis have prospects for the development of new cancer treatments. However, the design ideas of nanomaterials targeting ferroptosis sometimes vary. Therefore, in addition to the need for a systematic summary of these ideas, new ideas and insights are needed to make possible the construction of nanomaterials for effectively targeting this cell death pathway. At the same time, further optimization of nanomaterials design is required to make them appropriate for clinical treatment. In this context, we summarize this cross-cutting research area covering from the known mechanism of ferroptosis to providing feasible ideas for nanomaterials design as well as their clinical application. We aim to provide new insights and enlightenment for the next step in developing new nanomaterials for cancer treatment.

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Oxygenated phosphatidylethanolamine navigates phagocytosis of ferroptotic cells by interacting with TLR2

Cited by 154 publications

References 47 publications

Ferroptosis in infection, inflammation, and immunity

Ferroptosis in infection, inflammation, and immunity

The Phagocytic Code Regulating Phagocytosis of Mammalian Cells

Targeting ferroptosis-based cancer therapy using nanomaterials: strategies and applications

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