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Neutrophils, as primary responders to liver injury, undergo NETosis\u2014an immune response generating neutrophil extracellular traps (NETs), further amplifying inflammatory damage. Extracellular DNA (ecDNA), a major constituent of NETs and released cell fragments, potentiates inflammation through pattern recognition receptor activation. Mitochondrial DNA, released during hepatocyte damage, especially provokes robust immune responses due to its bacterial DNA-like structure and unmethylated CpG motifs. Concurrently, purinergic signaling\u2014particularly via ATP release and its conversion into adenosine by ectonucleotidases CD39 and CD73\u2014critically modulates immune homeostasis and inflammatory responses. Dysregulated expression of CD39\/CD73, driven by altered aryl hydrocarbon receptor (AhR) signaling, exacerbates inflammatory states through disturbed regulatory T (Treg) and T helper (Th) 17 cell balance. Recent insights highlight that neutrophils and NETs not only drive innate inflammatory responses but significantly influence adaptive immunity by modulating T cell differentiation. NET components, such as cathelicidin and histones, actively promote Th17 differentiation while simultaneously impairing Treg functions, thereby sustaining inflammatory conditions. In addition, T cells reciprocally influence neutrophil activation and recruitment, predominantly through interleukin-17A (IL-17A) production. Detailed mechanisms underlying neutrophil-T cell cross talk in autoimmune hepatitis, acute liver failure, ischemia\/reperfusion injury, alcoholic liver disease, and metabolic dysfunction-associated steatotic liver disease underscore potential therapeutic targets. 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