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Galectin-1 induces macrophage immunometabolic reprogramming, modulates T cell immunity and attenuates atherosclerotic plaque formation.
Atherosclerosis 413:120608 (2025)
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Forschungsdaten
DOI
PMC
BACKGROUND AND AIMS: Atherosclerosis is a chronic immunometabolic disease driven by lipid accumulation and immune cell infiltration. Macrophages and T cells play key roles throughout plaque development. Galectin-1 (Gal-1), a glycan-binding protein, modulates immune functions in these cells and has been reported to attenuate atherosclerosis, though its mechanisms remain incompletely understood. Here, we investigated the effects of Gal-1 on macrophages and T cells during plaque formation. METHODS: Effects of Gal-1 on atherosclerosis, macrophages and T cells during lesion formation were studied in Apoe-/- mice treated with recombinant Gal-1. Complementary mouse peritoneal foam cell and in vitro macrophage and T cell culture experiments were performed to study T cell differentiation, macrophage function, polarization and energy metabolism. The impact of Gal-1 on human macrophages was further evaluated in endarterectomy specimens. RESULTS: Gal-1 treatment reduced lesion size and increased circulating IL-10 levels, inversely correlating with plaque burden. Unexpectedly, IL-10 neutralization also mitigated atherosclerosis, indicating that its action is at least partially IL-10-independent. In plaques, Gal-1 promoted anti-inflammatory macrophage phenotypes, mirrored by a quiescent metabolic and anti-inflammatory profile in foamy macrophages ex vivo. The use of the Gal-1E71Q variant revealed that these effects were only partly dependent on glycan binding. Beyond IL-10, Gal-1 reshaped cytokine profiles by increasing IL-17, IL-22, and IL-23, consistent with a macrophage-driven regulatory Th17 response, alongside higher frequencies of IL-10-producing and regulatory T cells. CONCLUSION: Gal-1 protects against atherosclerosis associated with reprogramming macrophages and tuning T cell immunity through glycan-dependent and -independent pathways.
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Publikationstyp
Artikel: Journalartikel
Dokumenttyp
Wissenschaftlicher Artikel
Schlagwörter
Cytokine ; Foam Cell ; Glycan ; Glycolysis ; Macrophage Polarization ; Oxphos ; Treg
ISSN (print) / ISBN
0021-9150
e-ISSN
1879-1484
Zeitschrift
Atherosclerosis
Quellenangaben
Band: 413,
Artikelnummer: 120608
Verlag
Elsevier
Verlagsort
Amsterdam
Begutachtungsstatus
Peer reviewed
Institut(e)
Institute of Diabetes and Cancer (IDC)