ArticleProceedings of the National Academy of Sciences of the United States of America2016
Transcription factor KLF2 regulates homeostatic NK cell proliferation and survival.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 74 citations in OpenAlex.
- Rbp-Jκ controls NK cell late maturation and migration via chromatin landscape remodeling.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Maternal Krüppel-like factor 2 (KLF2)+ CD4 T cells promote fertility and fetal tolerance.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Transcriptional networks weaving natural killer anti-tumor immune response.Molecular cancer · 2026Review
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- Identification of ferroptosis-related genes involved in chronic obstructive pulmonary disease based on bioinformatics analysis.Animal models and experimental medicine · 2025Article
- TF Profiler: a transcription factor inference method that broadly measures transcription factor activity and identifies mechanistically distinct networks.Genome biology · 2025Article
- Interleukin-21 engineering enhances NK cell activity against glioblastoma via CEBPD.Cancer cell · 2024Article
- Pan-cancer profiling of tumor-infiltrating natural killer cells through transcriptional reference mapping.Nature immunology · 2024Article
- Eomesodermin spatiotemporally orchestrates the early and late stages of NK cell development by targeting KLF2 and T-bet, respectively.Cellular & molecular immunology · 2024Article
- Cytokines drive the formation of memory-like NK cell subsets via epigenetic rewiring and transcriptional regulation.Science immunology · 2024Article
- Rapid functional impairment of natural killer cells following tumor entry limits anti-tumor immunity.Nature communications · 2024Article
- Insights into the heterogeneity of iNKT cells: tissue-resident and circulating subsets shaped by local microenvironmental cues.Frontiers in immunology · 2024Review
- Transcription factor KLF2 is associated with the dysfunctional status of NK cells and the prognosis of pediatric B-ALL patients.Frontiers in oncology · 2024Article
- T-BET and EOMES sustain mature human NK cell identity and antitumor function.The Journal of clinical investigation · 2023Article
- KLF2 is a clinical diagnostic and treatment biomarker of breast cancer.Frontiers in cell and developmental biology · 2023Article
- Krüppel-like factors in tumors: Key regulators and therapeutic avenues.Frontiers in oncology · 2023Review
- Tissue-specific transcriptional profiles and heterogeneity of natural killer cells and group 1 innate lymphoid cells.Cell reports. Medicine · 2022Article
- The transcription factor Bach2 negatively regulates murine natural killer cell maturation and function.eLife · 2022Article
- KLF2-induced circZKSCAN1 potentiates the tumorigenic properties of clear cell renal cell carcinoma by targeting the miR-1294/PIM1 axis.Cell cycle (Georgetown, Tex.) · 2022Article
- Reprogramming the tumor microenvironment by genome editing for precision cancer therapy.Molecular cancer · 2022Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Natural killer (NK) cells are innate lymphocytes that recognize and lyse virally infected or transformed cells. This latter property is being pursued in clinics to treat leukemia with the hope that further breakthroughs in NK cell biology can extend treatments to other cancers. At issue is the ability to expand transferred NK cells and prolong their functionality within the context of a tumor. In terms of NK cell expansion and survival, we now report that Kruppel-like factor 2 (KLF2) is a key transcription factor that underpins both of these events. Excision of Klf2 using gene-targeted mouse models promotes spontaneous proliferation of immature NK cells in peripheral tissues, a phenotype that is replicated under ex vivo conditions. Moreover, KLF2 imprints a homeostatic migration pattern on mature NK cells that allows these cells to access IL-15-rich microenvironments. KLF2 accomplishes this feat within the mature NK cell lineage via regulation of a subset of homing receptors that respond to homeostatic ligands while leaving constitutively expressed receptors that recognize inflammatory cytokines unperturbed. Under steady-state conditions, KLF2-deficient NK cells alter their expression of homeostatic homing receptors and subsequently undergo apoptosis due to IL-15 starvation. This novel mechanism has implications regarding NK cell contraction following the termination of immune responses including the possibility that retention of an IL-15 transpresenting support system is key to extending NK cell activity in a tumor environment.
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