ArticleProceedings of the National Academy of Sciences of the United States of America2018
Tim-3 co-stimulation promotes short-lived effector T cells, restricts memory precursors, and is dispensable for T cell exhaustion.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 108 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
108 citing papers in PubMed, 1 synthesis or guideline pooled it, 168 citations in OpenAlex.
- An Emerging Role of TIM3 Expression on T Cells in Chronic Kidney Inflammation.Frontiers in immunology · 2021Pooled it
- TQB2618 plus Penpulimab, Alone or in Combination with Chemotherapy, for Recurrent or Metastatic Nasopharyngeal Carcinoma: A Multicenter, Two-Cohort, Phase II Trial.Clinical cancer research : an official journal of the American Association for Cancer Research · 2026Trial
- The multifaceted landscape of T cell exhaustion in organ transplantation: From molecular mechanisms (epigenetics, transcription, metabolism) to induction strategies.Genes & diseases · 2026Review
- TIM-3 in Cardiovascular Disease.Current heart failure reports · 2026Review
- Immune checkpoint molecules beyond PD-1 and CTLA-4: emerging targets in autoimmune diseases and cancer immunotherapy.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- A Predictive Immunological Signature Associated with Pathological Response in Breast Cancer Treated with Neoadjuvant Chemotherapy.Biomedicines · 2026Article
- Comparable restimulation of human T cells activated with CD3/CD28 beads versus soluble antibody complexes.Scientific reports · 2026Article
- Multi-omic profiling and preclinical efficacy of fratricide-driven, unedited CD7 CAR-T cells in T-cell leukemia.Journal of translational medicine · 2026Article
- The role of the TIM-3 receptor in inflammatory bowel disease and autoimmunity: implications for TIM-3 and TCR crosstalk.Journal of molecular medicine (Berlin, Germany) · 2026Review
- Plying potency assays for immunotherapy of solid tumors.Frontiers in immunology · 2026Review
- The Myeloid-T Lymphocyte Axis in Chronic Lung Allograft Rejection: Emerging Insights into the Immune Circuitry Driving Fibrosis.Results and problems in cell differentiation · 2026Review
- Unraveling the Role of Azobenzene-Based Photoswitchable Lipids in Controlling Innate Immune Response.Chemistry (Weinheim an der Bergstrasse, Germany) · 2025Article
- Soluble TIM-3 and galectin-9 predict survival in gastric and gastroesophageal junction cancer.iScience · 2025Article
- CD226 identifies effector CD8Cell reports · 2025Article
- Emerging new immune checkpoint inhibitors in solid tumor immunotherapy.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Lymphatic chain gradients regulate the magnitude and heterogeneity of T cell responses to vaccination.The Journal of experimental medicine · 2025Article
- The role of Tim-3+T cell subsets in the peripheral blood of patients with COVID-19 and diabetes.iScience · 2025Article
- Construction and validation of a reliable disulfidptosis-related lncRNAs signature of the subtype, prognostic, and immune landscape in bladder cancer.Discover oncology · 2025Article
- Oncolytic reprogramming of tumor microenvironment shapes CD4 T-cell memory via the IL6ra-Bcl6 axis for targeted control of glioblastoma.Nature communications · 2025Article
- Combined PARP14 inhibition and PD-1 blockade promotes cytotoxic T cell quiescence and modulates macrophage polarization in relapsed melanoma.Journal for immunotherapy of cancer · 2025Article
48 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Tim-3 is highly expressed on a subset of T cells during T cell exhaustion in settings of chronic viral infection and tumors. Using lymphocytic choriomeningitis virus (LCMV) Clone 13, a model for chronic infection, we found that Tim-3 was neither necessary nor sufficient for the development of T cell exhaustion. Nonetheless, expression of Tim-3 was sufficient to drive resistance to PD-L1 blockade therapy during chronic infection. Strikingly, expression of Tim-3 promoted the development of short-lived effector T cells, at the expense of memory precursor development, after acute LCMV infection. These effects were accompanied by increased Akt/mTOR signaling in T cells expressing endogenous or ectopic Tim-3. Conversely, Akt/mTOR signaling was reduced in effector T cells from Tim-3-deficient mice. Thus, Tim-3 is essential for optimal effector T cell responses, and may also contribute to exhaustion by restricting the development of long-lived memory T cells. Taken together, our results suggest that Tim-3 is actually more similar to costimulatory receptors that are up-regulated after T cell activation than to a dominant inhibitory protein like PD-1. These findings have significant implications for the development of anti-Tim-3 antibodies as therapeutic agents.
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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.