ArticleCell reports2023
Galectin-3 expression in donor T cells reduces GvHD severity and lethality after allogeneic hematopoietic cell transplantation.
Article in Cell reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 9 citations in OpenAlex.
- Galectin-3 restrains T cell-driven inflammation in the testis and epididymis.Cell death & disease · 2026Article
- The impact of T cell exhaustion in hematopoietic stem cell transplantation.Stem cell research & therapy · 2026Review
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- Article
- Altered distribution of tissue galectins correlates with mucosal dysregulation in SIV infection.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- Targeting the pentose phosphate pathway mitigates graft-versus-host disease by rewiring alloreactive T cell metabolism.JCI insight · 2025Article
- Current status, challenges, and integration pathways of biomarker classification systems in graft-versus-host disease: a preliminary exploration.Frontiers in medicine · 2025Review
- Intracellular galectin interactions in health and disease.Seminars in immunopathology · 2024Review
- Galectin-3 predicts acute GvHD and overall mortality post reduced intensity allo-HCT: a BMT-CTN biorepository study.Bone marrow transplantation · 2024Article
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Authors and funding
15 authors at 2 institutions in 1 country.
Funding
Abstract
Abundant donor cytotoxic T cells that attack normal host organs remain a major problem for patients receiving allogeneic hematopoietic cell transplantation (allo-HCT). Despite an increase in our knowledge of the pathobiology of acute graft versus host disease (aGvHD), the mechanisms regulating the proliferation and function of donor T cells remain unclear. Here, we show that activated donor T cells express galectin-3 (Gal-3) after allo-HCT. In both major and minor histocompatibility-mismatched models of murine aGvHD, expression of Gal-3 is associated with decreased T cell activation and suppression of the secretion of effector cytokines, including IFN-γ and GM-CSF. Mechanistically, Gal-3 results in activation of NFAT signaling, which can induce T cell exhaustion. Gal-3 overexpression in human T cells prevents severe disease by suppressing cytotoxic T cells in xenogeneic aGvHD models. Together, these data identify the Gal-3-dependent regulatory pathway in donor T cells as a critical component of inflammation in aGvHD.
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Registered trials
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