ArticleProceedings of the National Academy of Sciences of the United States of America2016
Multiple layers of transcriptional regulation by PLZF in NKT-cell development.
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 60 papers.
What it found
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Who cites it
60 citing papers in PubMed, 107 citations in OpenAlex.
- A common transcriptomic program acquired in the thymus defines tissue residency of MAIT and NKT subsets.The Journal of experimental medicine · 2019Trial
- CD23 sustains NKT17 cell homeostasis via IL-7Rα-mTORC2 signaling.Cell death & disease · 2026Article
- Maternal Obesity Reprograms Differentiation Trajectories of Fetal Hematopoietic Stem and Progenitor Cells Through Altered Inflammatory Signaling.bioRxiv : the preprint server for biology · 2026Article
- Spatially microdissected profiling of tonsillar germinal centers reveals a KLRG1-enriched immune signature in IgA nephropathy.Frontiers in immunology · 2026Article
- The glucocorticoid receptor is affected by its target ZBTB16 in a dissociated manner.The Journal of endocrinology · 2025Article
- Old versus new: upstream and downstream of promyelocytic leukemia zinc finger protein.Cancer gene therapy · 2025Review
- Primordial Cells Bridging the Gap Between Innate and Adaptive Immunity.Advances in experimental medicine and biology · 2025Review
- Generation of dual-attribute iTNK cells from hPSCs for cancer immunotherapy.Cell reports methods · 2024Article
- NKT Cells and Other Innate T Cells: The Immune Cells That Do Not Follow the Rules.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
- Establishment of Murine Pregnancy Requires the Promyelocytic Leukemia Zinc Finger Transcription Factor.International journal of molecular sciences · 2024Article
- A conserved transcriptional program for MAIT cells across mammalian evolution.The Journal of experimental medicine · 2024Article
- Transcriptional re-programming of liver-resident iNKT cells into T-regulatory type-1-like liver iNKT cells involves extensive gene de-methylation.Frontiers in immunology · 2024Article
- Luminal breast cancer identity is determined by loss of glucocorticoid receptor activity.EMBO molecular medicine · 2023Article
- Article
- Invariant natural killer T cells in lung diseases.Experimental & molecular medicine · 2023Review
- Enhanced ZBTB16 Levels by Progestin-Only Contraceptives Induces Decidualization and Inflammation.International journal of molecular sciences · 2023Article
- Role of MR1-driven signals and amphiregulin on the recruitment and repair function of MAIT cells during skin wound healing.Immunity · 2023Article
- Unconventional T cells in brain homeostasis, injury and neurodegeneration.Frontiers in immunology · 2023Review
- Progranulin regulates the development and function of NKT2 cells through EZH2 and PLZF.Cell death and differentiation · 2022Article
- Pla2g2a promotes innate Th2-type immunity lymphocytes to increase B1a cells.Scientific reports · 2022Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
The transcription factor PLZF [promyelocytic leukemia zinc finger, encoded by zinc finger BTB domain containing 16 (Zbtb16)] is induced during the development of innate and innate-like lymphocytes to direct their acquisition of a T-helper effector program, but the molecular mechanisms involved are poorly understood. Using biotinylation-based ChIP-seq and microarray analysis of both natural killer T (NKT) cells and PLZF-transgenic thymocytes, we identified several layers of regulation of the innate-like NKT effector program. First, PLZF bound and regulated genes encoding cytokine receptors as well as homing and adhesion receptors; second, PLZF bound and activated T-helper-specific transcription factor genes that in turn control T-helper-specific programs; finally, PLZF bound and suppressed the transcription of Bach2, a potent general repressor of effector differentiation in naive T cells. These findings reveal the multilayered architecture of the transcriptional program recruited by PLZF and elucidate how a single transcription factor can drive the developmental acquisition of a broad effector program.
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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.