ArticleThe Journal of experimental medicine2026
IFNγ-induced memory in human macrophages is sustained by the durability of cytokine signaling itself.
Article in The Journal of experimental medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Epigenetic profiling reveals M1 macrophages as the primary drivers of trained immunity in HSV-1 latently infected mice.PLoS pathogens · 2026Article
- 1 Hz Low-Frequency Repetitive Transcranial Magnetic Stimulation Ameliorates Epilepsy by Suppressing Interferon-γ Signaling-Dependent Microglial Synaptic Phagocytosis in Mice.CNS neuroscience & therapeutics · 2026Article
- Integrated multi-omics analysis reveals shared IFN-γ-associated monocyte signatures in primary Sjögren's syndrome and Alzheimer's disease.Frontiers in immunology · 2026Article
- Cross-Talk Between Neutrophils and Macrophages Post-Myocardial Infarction: From Inflammatory Drivers to Therapeutic Targets.International journal of molecular sciences · 2025Review
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
Macrophages, as key sentinel cells of the innate immune system, can retain memory of prior stimulus exposure. IFNγ plays a central role in maintaining trained immunity in vivo and can induce potent memory in macrophages. Such memory is associated with the formation of de novo enhancers that alter gene expression responses to subsequent stimuli. However, how such enhancers are maintained after cytokine exposure remains unclear. We report that the mechanism underlying durable IFNγ-induced enhancers is not cell intrinsic. IFNγ-treated macrophages continue to exhibit JAK/STAT signaling days after cytokine removal. Blocking IFNγ signaling with a JAK inhibitor or anti-IFNγ neutralizing antibodies after cytokine removal is sufficient to reverse IFNγ-induced enhancers and erase the potentiated state of the treated macrophages. Our findings suggest that epigenetic changes in macrophages do not inherently encode innate immune memory or a "potentiated" macrophage state, but in fact are themselves dependent on ongoing signaling from cytokines sequestered at the cell surface.
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Registered trials
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