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CD8+ T cells and fatty acids orchestrate tumor ferroptosis and immunity via ACSL4 - ScienceDirect
Source: sciencedirect.com
Article summary:
1. CD8+ T cells and arachidonic acid (AA) induce tumor ferroptosis via ACSL4: The study reveals that the combination of CD8+ T cell-derived interferon (IFN)γ and AA triggers immunogenic tumor ferroptosis through the activation of ACSL4, a key enzyme involved in lipid metabolism. This finding suggests that CD8+ T cells play a crucial role in initiating tumor cell death through ferroptosis.
2. ACSL4 mediates immunogenic tumor ferroptosis: The researchers demonstrate that ACSL4 is responsible for mediating immunogenic tumor ferroptosis by altering the lipid composition of tumor cells. Specifically, IFNγ stimulates ACSL4 expression and increases the incorporation of AA into specific phospholipids, leading to enhanced ferroptotic cell death.
3. Targeting tumor ACSL4 enhances anti-tumor immunity: The study shows that targeting ACSL4 sensitizes checkpoint therapy and improves anti-tumor immune responses. Low-dose AA treatment promotes tumor ferroptosis and enhances both spontaneous and immune checkpoint blockade-induced anti-tumor immunity. Additionally, clinical data indicates that high ACSL4 expression correlates with improved survival in cancer patients treated with immune checkpoint blockade therapy.
Overall, this research highlights the importance of CD8+ T cells, fatty acids, and ACSL4 in orchestrating tumor ferroptosis and immune responses, suggesting that targeting the ACSL4 pathway could be a potential therapeutic strategy for cancer treatment.
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