ReviewJournal of inflammation research2026
The Dual Role of Natural Killer Cells in the Septic Liver.
Review in Journal of inflammation research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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0 citing papers in PubMed.
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sepsis is a life-threatening organ dysfunction caused by dysregulated host responses to infection. As an important immune organ, the liver plays a vital role in the pathophysiological process of sepsis. When sepsis occurs, the liver exhibits unique immunological characteristics, including abnormal activation of pattern recognition receptors, loss of control of the complement system, adaptive immune regulation, and hepatic Kupffer cell polarization, which together determine the outcome of septic liver. Natural killer (NK) cells are innate immune cells with different biological characteristics in the liver than circulating NK cells. Natural killer (NK) cells assume a dual role in hepatic pathophysiology, functioning as both protectors and effectors of injury. On the protective front, these cells mediate antimicrobial defense and immunomodulation through interferon-gamma (IFN-γ) secretion, maintain vascular endothelial barrier integrity via vascular endothelial growth factor (VEGF) downregulation, and regulate hepatic inflammation through the production of anti-inflammatory cytokines such as interleukin-10 (IL-10). Additionally, their cytotoxic activity effectively suppresses viral replication within the hepatic microenvironment. Conversely, NK cells contribute to hepatocellular damage through distinct deleterious mechanisms. They elaborate tumor necrosis factor-alpha (TNF-α) and IFN-γ, thereby precipitating cytokine storm formation. Through the exogenous pathway (Fas ligand/TNF-related apoptosis-inducing ligand [FasL/TRAIL]) and the endogenous pathway (perforin/granzyme), they directly induce hepatocyte apoptosis. Furthermore, NK cells regulate ferroptosis-related gene expression-including heme oxygenase-1 (Hmox1) and solute carrier family 3 member 2 (Slc3a2)-thus driving the progression of sepsis-associated liver failure. This review describes the immunological characteristics of the liver in sepsis and the mechanisms of NK protection and damage to the liver. This study provides a new perspective for exploring immunotherapy of septic liver injury in the future.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.