ArticleProceedings of the National Academy of Sciences of the United States of America2016
Transcription factor Bcl11b sustains iNKT1 and iNKT2 cell programs, restricts iNKT17 cell program, and governs iNKT cell 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 19 papers.
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19 citing papers in PubMed, 25 citations in OpenAlex.
- A novel heterozygous mutation of BCL11B gene causes neurodevelopmental disorder and middle type hypospadias in a Chinese boy with 5 years follow-up.Neurogenetics · 2026Article
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- Myeloid/natural killer (NK) cell precursor acute leukemia as a distinct leukemia type.Science advances · 2023Article
- Markers and makers of NKT17 cells.Experimental & molecular medicine · 2023Review
- Bcl11b sustains multipotency and restricts effector programs of intestinal-resident memory CD8Science immunology · 2023Article
- Modulation of TCR signalling components occurs prior to positive selection and lineage commitment in iNKT cells.Scientific reports · 2021Article
- Article
- The transcription factor Bcl11b promotes both canonical and adaptive NK cell differentiation.Science immunology · 2021Article
- Epigenetic Dynamics in the Function of T-Lineage Regulatory Factor Bcl11b.Frontiers in immunology · 2021Review
- Bcl11b/Ctip2 in Skin, Tooth, and Craniofacial System.Frontiers in cell and developmental biology · 2020Review
- Coexpression of YY1 Is Required to Elaborate the Effector Functions Controlled by PLZF in NKT Cells.Journal of immunology (Baltimore, Md. : 1950) · 2019Article
- Bcl11b prevents fatal autoimmunity by promoting TScience advances · 2019Article
- Bcl11b sets pro-T cell fate by site-specific cofactor recruitment and by repressing Id2 and Zbtb16.Nature immunology · 2018Article
- Bcl11b is essential for licensing Th2 differentiation during helminth infection and allergic asthma.Nature communications · 2018Article
- Invariant Natural Killer T Cell Subsets-More Than Just Developmental Intermediates.Frontiers in immunology · 2018Review
- The differentiation of ROR-γt expressing iNKT17 cells is orchestrated by Runx1.Scientific reports · 2017Article
- TET proteins regulate the lineage specification and TCR-mediated expansion of iNKT cells.Nature immunology · 2017Article
- Unraveling Natural Killer T-Cells Development.Frontiers in immunology · 2017Review
- Transcription Factor Bcl11b Controls Effector and Memory CD8 T cell Fate Decision and Function during Poxvirus Infection.Frontiers in immunology · 2016Article
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Invariant natural killer T (iNKT) cells are innate-like T cells that recognize glycolipid antigens and play critical roles in regulation of immune responses. Based on expression of the transcription factors (TFs) Tbet, Plzf, and Rorγt, iNKT cells have been classified in effector subsets that emerge in the thymus, namely, iNKT1, iNKT2, and iNKT17. Deficiency in the TF Bcl11b in double-positive (DP) thymocytes has been shown to cause absence of iNKT cells in the thymus and periphery due to defective self glycolipid processing and presentation by DP thymocytes and undefined intrinsic alterations in iNKT precursors. We used a model of cre-mediated postselection deletion of Bcl11b in iNKT cells to determine its intrinsic role in these cells. We found that Bcl11b is expressed equivalently in all three effector iNKT subsets, and its removal caused a reduction in the numbers of iNKT1 and iNKT2 cells, but not in the numbers of iNKT17 cells. Additionally, we show that Bcl11b sustains subset-specific cytokine production by iNKT1 and iNKT2 cells and restricts expression of iNKT17 genes in iNKT1 and iNKT2 subsets, overall restraining the iNKT17 program in iNKT cells. The total numbers of iNKT cells were reduced in the absence of Bcl11b both in the thymus and periphery, associated with the decrease in iNKT1 and iNKT2 cell numbers and decrease in survival, related to changes in survival/apoptosis genes. Thus, these results extend our understanding of the role of Bcl11b in iNKT cells beyond their selection and demonstrate that Bcl11b is a key regulator of iNKT effector subsets, their function, identity, and survival.
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