ArticleProceedings of the National Academy of Sciences of the United States of America2011
Transcription factor Bcl11b controls selection of invariant natural killer T-cells by regulating glycolipid presentation in double-positive thymocytes.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 46 citations in OpenAlex.
- Targeting BCL11B in CAR-engineered lymphoid progenitors drives NK-like cell development with prolonged anti-leukemic activity.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- A mutant BCL11B-N440K protein interferes with BCL11A function during T lymphocyte and neuronal development.Nature immunology · 2024Article
- Functional overlap of inborn errors of immunity and metabolism genes defines T cell metabolic vulnerabilities.Science immunology · 2024Article
- A Bcl11bFrontiers in immunology · 2024Article
- Bcl11b sustains multipotency and restricts effector programs of intestinal-resident memory CD8Science immunology · 2023Article
- Construction of ovarian metastasis-related immune signature predicting prognosis of gastric cancer patients.Cancer medicine · 2023Article
- The histone demethylase Lsd1 regulates multiple repressive gene programs during T cell development.The Journal of experimental medicine · 2021Article
- Article
- The transcription factor Bcl11b promotes both canonical and adaptive NK cell differentiation.Science immunology · 2021Article
- Retroviral Transduction of NKT Hybridoma Cells.Methods in molecular biology (Clifton, N.J.) · 2021Article
- Case Report and Review of the Literature: Congenital Diaphragmatic Hernia and Craniosynostosis, a Coincidence or Common Cause?Frontiers in pediatrics · 2021Article
- Bcl11b/Ctip2 in Skin, Tooth, and Craniofacial System.Frontiers in cell and developmental biology · 2020Review
- Bcl11b prevents fatal autoimmunity by promoting TScience advances · 2019Article
- A de novo substitution in BCL11B leads to loss of interaction with transcriptional complexes and craniosynostosis.Human molecular genetics · 2019Article
- Bcl11b is essential for licensing Th2 differentiation during helminth infection and allergic asthma.Nature communications · 2018Article
- How Lipid-Specific T Cells Become Effectors: The Differentiation of iNKT Subsets.Frontiers in immunology · 2018Review
- Priming of lineage-specifying genes by Bcl11b is required for lineage choice in post-selection thymocytes.Nature communications · 2017Article
- Transcription factor Bcl11b sustains iNKT1 and iNKT2 cell programs, restricts iNKT17 cell program, and governs iNKT cell survival.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Transcription Factor Bcl11b Controls Effector and Memory CD8 T cell Fate Decision and Function during Poxvirus Infection.Frontiers in immunology · 2016Article
- Forging T-Lymphocyte Identity: Intersecting Networks of Transcriptional Control.Advances in immunology · 2016Review
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Authors and funding
8 authors at 3 institutions in 3 countries.
Funding
Abstract
Invariant natural killer T cells (iNKT cells) are innate-like T cells important in immune regulation, antimicrobial protection, and anti-tumor responses. They express semi-invariant T cell receptors, which recognize glycolipid antigens. Their positive selection is mediated by double-positive (DP) thymocytes, which present glycolipid self-antigens through the noncanonical MHC class I-like molecule CD1d. Here we provide genetic and biochemical evidence that removal of the transcription factor Bcl11b in DP thymocytes leads to an early block in iNKT cell development, caused by both iNKT cell extrinsic and intrinsic defects. Specifically, Bcl11b-deficient DP thymocytes failed to support Bcl11b-sufficient iNKT precursor development due to defective glycolipid self-antigen presentation, and showed enlarged lysosomes and accumulation of glycosphingolipids. Expression of genes encoding lysosomal proteins with roles in sphingolipid metabolism and glycolipid presentation was found to be altered in Bcl11b-deficient DP thymocytes. These include cathepsins and Niemann-Pick disease type A, B, and C genes. Thus, Bcl11b plays a central role in presentation of glycolipid self-antigens by DP thymocytes, and regulates directly or indirectly expression of lysosomal genes, exerting a critical extrinsic role in development of iNKT lineage, in addition to the intrinsic role in iNKT precursors. These studies demonstrate a unique and previously undescribed role of Bcl11b in DP thymocytes, in addition to the critical function in positive selection of conventional CD4 and CD8 single-positive thymocytes.
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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.