ReviewFrontiers in immunology2026
Metabolic licensing at the dendritic cell-NK cells immune synapse in viral asthma exacerbations.
Review in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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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Who cites it
1 citing paper in PubMed.
- Glycolytic reprogramming and cell-specific lactylation in asthma: an evidence-graded framework for testable metabolic-epigenetic profiles.Frontiers in immunology · 2026Review
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Asthma exacerbations are predominantly triggered by respiratory viral infections, yet current therapies largely fail to restore effective antiviral immunity. Emerging data indicate that this failure is tightly coupled to dysregulated immunometabolism within the asthmatic lung. This review advances the concept of a dendritic cell-natural killer (DC-NK) metabolic checkpoint, whereby the metabolic state of DCs, regulated by autophagy and AMPK/mTOR signaling, licenses NK cells for antiviral effector function. In type 2-high, type 2-low, and obesity-related asthma endotypes, chronic hypoxia, HIF-1α stabilization, ORMDL3-ceramide signaling, and systemic metabolic stress converge to induce highly glycolytic, Th2/Th17-polarizing DCs in a lactate-rich, acidic microenvironment. We propose that these DCs modulate NK cell metabolism through three interlinked axes: (i) cytokine-mediated metabolic licensing (IL-12, IL-15, IL-18), (ii) exosome-mediated delivery of activating versus metabolically suppressive cargo, and (iii) intense perisynaptic nutrient competition that depletes local glucose while lactate accumulation and acidosis further inhibit NK cell function. The result is a "double metabolic hit" that renders lung-resident NK cells metabolically exhausted, IFN-γ-deficient, and unable to clear virally infected targets despite preserved cytotoxic machinery. Although many mechanistic insights derive from murine and
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