ArticleProceedings of the National Academy of Sciences of the United States of America2025
Galectin-9 binding to HLA-DR in dendritic cells controls immune synapse formation and T cell proliferation.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2025. 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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Decoding Treg diversity and dysfunction to advance Treg-based therapies in autoimmune and inflammatory diseases.Frontiers in immunology · 2026Review
Corrections and comments
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Authors and funding
17 authors.
Funding
Abstract
To initiate T cell-mediated immunity, dendritic cells (DCs) present antigens to T cells through the establishment of an immune synapse (IS). While events behind IS formation in T cells are well understood, the organization of IS components at the DC membrane remains ill-defined. Galectins modulate immune responses via glycan-(in)dependent interactions but the molecular mechanisms underlying their function in DC-mediated T cell activation, are poorly described. Here, we demonstrate that intracellular galectin-9 (gal9) in DCs is required for CD4
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.