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Metabolic-epigenetic rewiring of CCR5 hi monocytes sustains long-term trained immunity against lethal sepsis
Abstract INTRODUCTION RESULTS DISCUSSION MATERIALS AND METHODS Acknowledgments Supplementary Materials REFERENCES Information & Authors Metrics & Citations View Options References Figures Tables Media Share Abstract Trained immunity enhances innate host defense by endowing monocytes with memory-like properties, yet the underlying integrated metabolic and epigenetic mechanisms remain elusive.
Extracellular GPX4 impairs antitumor immunity via dendritic ZP3 receptors
Keywords cancer therapy cell death immunogenicity oxidative stress zona pellucida family Get full text access Log in, subscribe or purchase for full access. References 1. Chen, R. ∙ Zou, J. ∙ Liu, J. ... DAMPs in the immunogenicity of cell death Mol. Cell. 2025; 85:3874-3889 2. Kroemer, G. ∙ Galassi, C. ∙ Zitvogel, L. ... Immunogenic cell stress and death Nat. Immunol. 2022; 23:487-500 3. Tang, D. ∙ Kang, R. ∙ Berghe, T.V. ... The molecular machinery of regulated cell death Cell Res. 2019; 29:347-364 4. Ma, M.
BCG‐Derived Outer Membrane Vesicles Induce TLR2‐Dependent Trained Immunity to Protect Against Polymicrobial Sepsis (Adv. Sci. 37/2025)
Graphical Abstract Protection Against Polymicrobial Sepsis This artistic illustration depicts how Bacillus Calmette-Guérin (BCG) -derived outer membrane vesicles (OMVs) enhance host defenses by inducing trained immunity. Much like a fortified castle with reinforced walls and vigilant guards, the BCG-OMVs-trained host effectively repels microbial invaders, in contrast to untrained hosts vulnerable to polymicrobial sepsis.
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