{
  "abstract": "BackgroundGalectin-3 (Gal-3) is a multifunctional β-galactoside-binding lectin implicated in immune regulation, yet its association with T cell phenotypes under physiological and inflammatory conditions remains incompletely defined.MethodsWe investigated Gal-3 expression and binding on murine and human T cells across developmental stages, tissues, sex, genetic background, circadian time, and inflammatory disease settings.ResultsIn mice, Gal-3-associated CD4+ and CD8+ T cells were dynamically regulated by age, anatomical location, strain, sex, and circadian rhythm. Gal-3+ T cells displayed increased activation markers, enhanced TCR-associated signaling molecules, elevated cytolytic mediators, increased proliferation, and greater apoptosis. Gal-3+ T cells were enriched within central and effector memory compartments and expressed higher levels of co-inhibitory receptors, including PD-1, with ImageStream analysis confirming Gal-3 co-expressed with PD-1. Recombinant Gal-3 preferentially bound activated, but not resting T cells, and associated with CD44 and CD3, suggesting activation-dependent acquisition of extracellular Gal-3. Re-analysis of human thymocyte and Long COVID single-cell RNA-seq datasets further supported an association between LGALS3 expression and activated/exhausted T cell states. Finally, intracellular staining indicated that T cells are unlikely to be a major source of Gal-3.ConclusionOur findings identify Gal-3 as a context-dependent marker and potential regulator of activated, antigen-experienced T cells, which promotes T cell apoptosis.",
  "abstract_shown": true,
  "affiliations": [],
  "article_type": "Original Research",
  "arxiv": null,
  "author_total": 7,
  "authors": [
    {
      "name": "Amal Abouda"
    },
    {
      "name": "Emmanuel T. Alimo"
    },
    {
      "name": "Ako Azimi"
    },
    {
      "name": "AmirAli Bigleri"
    },
    {
      "name": "Amirhossein Rahmati"
    },
    {
      "name": "Shima Shahbaz"
    },
    {
      "name": "Shokrollah Elahi"
    }
  ],
  "bibtex": "https://research.draconitic.com/paper/f9wtxetp51vpc.bib",
  "cited_by": 0,
  "doi": "10.3389/fimmu.2026.1940192",
  "fulltext_url": null,
  "id": "f9wtxetp51vpc",
  "issns": [
    "1664-3224"
  ],
  "landing_url": "https://www.frontiersin.org/articles/10.3389/fimmu.2026.1940192",
  "language": null,
  "licence": "CC-BY-4.0",
  "licence_label": "CC BY 4.0",
  "licence_source": "article",
  "licence_url": "https://creativecommons.org/licenses/by/4.0/",
  "metadata_licence": null,
  "native_subjects": [
    [
      "feed-journal",
      "biology/immunology"
    ]
  ],
  "openalex": null,
  "pdf_url": null,
  "pmcid": null,
  "pmid": null,
  "published": "2026-11-04",
  "publisher": "Frontiers Media SA",
  "ris": "https://research.draconitic.com/paper/f9wtxetp51vpc.ris",
  "sources": [
    {
      "first_seen": "2026-11-04T06:20:39Z",
      "native_id": "10.3389/fimmu.2026.1940192",
      "source": "feed-frontiers",
      "url": "https://www.frontiersin.org/articles/10.3389/fimmu.2026.1940192"
    },
    {
      "first_seen": "2026-11-04T12:21:26Z",
      "native_id": "10.3389/fimmu.2026.1940192",
      "source": "crossref",
      "url": "https://www.frontiersin.org/articles/10.3389/fimmu.2026.1940192/full"
    }
  ],
  "subjects": [
    {
      "field": "biology",
      "origin": "feed-journal:biology/immunology",
      "subfield": "immunology"
    }
  ],
  "title": "Extracellular galectin-3 preferentially through CD44 and PD-1 binds activated T cells and marks memory-phenotype T cell subsets",
  "title_text": "Extracellular galectin-3 preferentially through CD44 and PD-1 binds activated T cells and marks memory-phenotype T cell subsets",
  "type": "peer-reviewed",
  "updated_at": "2026-11-04T12:21:26Z",
  "url": "https://research.draconitic.com/paper/f9wtxetp51vpc",
  "venue": "Frontiers in Immunology",
  "versions": []
}