ArticlePloS one2013
The impact of KLF2 modulation on the transcriptional program and function of CD8 T cells.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 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.
The trial behind it
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Who cites it
37 citing papers in PubMed, 46 citations in OpenAlex.
- CD8⁺ T Cell infiltration and spatial organization in cancer: mechanisms, barriers, and therapeutic strategies.Molecular biomedicine · 2026Review
- KLF2 overrides the resident memory CD8 T cell differentiation program, in opposition to KLF3.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Transient loss of KLF2 expression is essential for CD8 effector T cell expansion.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- Review
- HIV infection reprogrammes CD4+ T cells for quiescence and entry into proviral latency.Nature microbiology · 2025Article
- Guardians of silence: transcriptional networks in T cell quiescence.Experimental & molecular medicine · 2025Review
- CNS Involvement by North American-Adult T-cell Leukemia/Lymphoma Is Associated With Discrete Dissemination Patterns and Molecular Profiles, Involving XPO1 E571 and KLF2/PI3KCD in Selected Cases.JCO precision oncology · 2025Article
- KLF2 maintains lineage fidelity and suppresses CD8 T cell exhaustion during acute LCMV infection.Science (New York, N.Y.) · 2025Article
- Epigenetic control of tissue resident memory T cells.Frontiers in immunology · 2025Review
- Construction and validation of transcription‑factor‑based prognostic signature for TACE non‑response and characterization of tumor microenvironment infiltration in hepatocellular carcinoma.Oncology letters · 2025Article
- CXCR3-CXCL11 Signaling Restricts Angiogenesis and Promotes Pericyte Recruitment.Arteriosclerosis, thrombosis, and vascular biology · 2024Article
- Prion protein alters viral control and enhances pathology after perinatal cytomegalovirus infection.Nature communications · 2024Article
- The role of circulating T cells with a tissue resident phenotype (ex-TFrontiers in immunology · 2024Review
- Egress of resident memory T cells from tissue with neoadjuvant immunotherapy: Implications for systemic anti-tumor immunity.Oral oncology · 2023Review
- CXCR3-CXCL11 signaling restricts angiogenesis and promotes pericyte recruitment.bioRxiv : the preprint server for biology · 2023Article
- Evaluating the transcriptional landscape and cell-cell communication networks in chronically irradiated parotid glands.iScience · 2023Article
- Chronic HCV infection promotes cytotoxicity in antigen-specific CD8Frontiers in virology (Lausanne, Switzerland) · 2023Article
- Transcriptomic Profiling Identifies CD8Journal of immunology (Baltimore, Md. : 1950) · 2022Article
- Review
- Nanoliposome C6-Ceramide in combination with anti-CTLA4 antibody improves anti-tumor immunity in hepatocellular cancer.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Krüppel-like factor 2 (KLF2) is a transcription factor that is highly expressed in quiescent T lymphocytes and downregulated in effector T cells. We now show that antigen receptor engagement downregulates KLF2 expression in a graded response determined by the affinity of T cell antigen receptor (TCR) ligand and the integrated activation of protein kinase B and the MAP kinases ERK1/2. The present study explores the importance of KLF2 downregulation and reveals that the loss of KLF2 controls a select portion of the CD8 effector T cell transcriptional program. In particular, KLF2 loss is required for CD8 T cells to express the inflammatory chemokine receptor CXCR3 and for maximum clonal expansion of T cells. KLF2 thus negatively controls the ability of CD8 T cells to respond to the CXCR3 ligand CXCL10. Strikingly, the KLF2 threshold for restraining expression of CXCR3 is very low and quite distinct to the KLF2 threshold for restraining T cell proliferation. KLF2 is thus an analogue (tunable) not a digital (on/off) cellular switch where the magnitude of KLF2 expression differentially modifies the T cell responses.
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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.