ArticleThe Biochemical journal2021
Phosphatidylserine binding directly regulates TIM-3 function.
Article in The Biochemical journal, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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.
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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.
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Who cites it
34 citing papers in PubMed, 53 citations in OpenAlex.
- Metabolic remodeling of endometriosis microenvironment: Energy stress and immune evasion.iScience · 2026Review
- Advancements in Immune Checkpoint-Based Immunotherapy for Triple-Negative Breast Cancer.Current issues in molecular biology · 2026Review
- Review
- TIM-3 in AML: a janus-faced orchestrator of immune exhaustion and leukemic self-renewal.Cancer cell international · 2026Review
- TIM-3 in Cardiovascular Disease.Current heart failure reports · 2026Review
- Multi-omic profiling and preclinical efficacy of fratricide-driven, unedited CD7 CAR-T cells in T-cell leukemia.Journal of translational medicine · 2026Article
- TIM-3+ Macrophages: Insights into Their Role in Cancer and Inflammation.International journal of molecular sciences · 2026Review
- Recent advances in preclinical studies combining hyperthermia therapy with novel immune checkpoint targeting agents.Frontiers in immunology · 2026Review
- Article
- TIM3-mediated differentiation of IL-10-producing CD25Journal of molecular medicine (Berlin, Germany) · 2025Article
- Post-translational modifications of cancer immune checkpoints: mechanisms and therapeutic strategies.Molecular cancer · 2025Review
- First-in-human phase I open-label study of the anti-TIM-3 monoclonal antibody INCAGN02390 in patients with select advanced or metastatic solid tumors.The oncologist · 2025Article
- Negative Immune Checkpoint Inhibitors.Pharmaceutics · 2025Review
- TIM-3 teams up with PD-1 in cancer immunotherapy: mechanisms and perspectives.Molecular biomedicine · 2025Review
- Serum soluble Tim‑3 is elevated in patients with cervical cancer and is higher in advanced clinical stages.Biomedical reports · 2025Article
- Reprogramming the breast tumor immune microenvironment: cold-to-hot transition for enhanced immunotherapy.Journal of experimental & clinical cancer research : CR · 2025Review
- Tissue factor-dependent colitogenic CD4Nature communications · 2025Article
- Pan-cancer analysis of co-inhibitory molecules revealing their potential prognostic and clinical values in immunotherapy.Frontiers in immunology · 2025Article
- TIM3 in COVID-19; A potential hallmark?Heliyon · 2024Review
- Tim-3 Is Required for Regulatory T Cell-Mediated Promotion of T Cell Exhaustion and Viral Persistence during Chronic Lymphocytic Choriomeningitis Virus Infection.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Co-signaling receptors for the T cell receptor (TCR) are important therapeutic targets, with blockade of co-inhibitory receptors such as PD-1 now central in immuno-oncology. Advancing additional therapeutic immune modulation approaches requires understanding ligand regulation of other co-signaling receptors. One poorly understood potential therapeutic target is TIM-3 (T cell immunoglobulin and mucin domain containing-3). Which of TIM-3's several proposed regulatory ligands is/are relevant for signaling is unclear, and different studies have reported TIM-3 as a co-inhibitory or co-stimulatory receptor in T cells. Here, we show that TIM-3 promotes NF-κB signaling and IL-2 secretion following TCR stimulation in Jurkat cells, and that this activity is regulated by binding to phosphatidylserine (PS). TIM-3 signaling is stimulated by PS exposed constitutively in cultured Jurkat cells, and can be blocked by mutating the PS-binding site or by occluding this site with an antibody. We also find that TIM-3 signaling alters CD28 phosphorylation. Our findings clarify the importance of PS as a functional TIM-3 ligand, and may inform the future exploitation of TIM-3 as a therapeutic target.
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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.