ArticleNature medicine2012
Bat3 promotes T cell responses and autoimmunity by repressing Tim-3–mediated cell death and exhaustion.
Article in Nature medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 246 papers, 1 of them a synthesis that pooled it.
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Who cites it
246 citing papers in PubMed, 1 synthesis or guideline pooled it, 374 citations in OpenAlex.
- An Emerging Role of TIM3 Expression on T Cells in Chronic Kidney Inflammation.Frontiers in immunology · 2021Pooled it
- Molecular Architecture and Clinical Landscape of Immune Checkpoint Receptors and Ligands.Antibodies (Basel, Switzerland) · 2026Review
- Protein Posttranslational Modifications in Immunity: Molecular Mechanisms and Therapeutic Targets.MedComm · 2026Review
- Extended HLA haplotypes and transplant survival.Blood · 2026Article
- Review
- Review
- TIM-3 in Cardiovascular Disease.Current heart failure reports · 2026Review
- TIM-3 in AML: pathogenic roles and therapeutic targetability.Clinical and experimental medicine · 2026Review
- Tim-3 agonist restrains ILC2 function and attenuates airway hyperreactivity via NLK pathway.Nature communications · 2026Article
- Immune checkpoint TIM-3 in tumor immunotherapy.Acta biochimica et biophysica Sinica · 2026Review
- Targeting T cell exhaustion in colorectal cancer: emerging roles of LAG-3, TIM-3, and TIGIT signaling in overcoming immunotherapy resistance.Cell communication and signaling : CCS · 2026Review
- Post-translational modifications of immune checkpoints: molecular mechanisms, tumor microenvironment remodeling, and therapeutic implications.Journal of biomedical science · 2026Review
- 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
- Fusion protein-mediated costimulation in engineered T cells: from intrinsic signaling to tumor microenvironment rewiring.Frontiers in immunology · 2026Review
- Identification of a novel inflammatory mast cell subpopulation in triple-negative breast cancer.Frontiers in immunology · 2026Article
- Dynamics of checkpoint receptors in γδ T cell subsets are associated with clinical response during anti-PD-1 immunotherapies.EMBO molecular medicine · 2026Article
- Soluble TIM-3 and galectin-9 predict survival in gastric and gastroesophageal junction cancer.iScience · 2025Article
- Recent progress in immune evasion mechanisms of triple-negative breast cancer.Journal of translational medicine · 2025Review
- High-throughput discovery of transmembrane helix dimers from human single-pass membrane proteins with TOXGREEN sort-seq.PNAS nexus · 2025Article
- New horizons in B-cell lymphoma immunotherapy: From immune checkpoints to precision medicine.Neoplasia (New York, N.Y.) · 2025Review
186 more citing papers are in PubMed but not listed here.
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Authors and funding
16 authors at 8 institutions in 2 countries.
Funding
Abstract
T cell immunoglobulin and mucin domain–containing 3 (Tim-3) is an inhibitory receptor that is expressed on exhausted T cells during infection with HIV-1 and hepatitis C virus. By contrast, Tim-3 expression and function are defective in multiple human autoimmune diseases. However, the molecular mechanisms modulating Tim-3 function are not well understood. Here we show that human leukocyte antigen B (HLA-B)-associated transcript 3 (Bat3) binds to, and represses the function of, Tim-3. Bat3 protects T helper type 1 (TH1) cells from galectin-9–mediated cell death and promotes both proliferation and proinflammatory cytokine production. Bat3-deficient T cells have elevated expression of exhaustion-associated molecules such as Tim-3, Lag3, Prdm1 and Pbx3, and Bat3 knockdown in myelin-antigen–specific CD4+ T cells markedly inhibits the development of experimental autoimmune encephalomyelitis while promoting the expansion of a dysfunctional Tim-3hi, interferon-γ (IFN-γ)loCD4+ cell population. Furthermore, expression of Bat3 is reduced in exhausted Tim-3+ T cells from mouse tumors and HIV-1–infected individuals. These data indicate that Bat3 acts as an inhibitor of Tim-3–dependent exhaustion and cell death. Bat3 may thus represent a viable therapeutic target in autoimmune disorders, chronic infections and cancers.
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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.