ArticleImmunity2015
Transcription Factor Bcl11b Controls Identity and Function of Mature Type 2 Innate Lymphoid Cells.
Article in Immunity, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 107 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.
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Who cites it
107 citing papers in PubMed, 177 citations in OpenAlex.
- Bcl11b dose-dependently regulates positive selection of CD8 T cells to the virtual memory fate.bioRxiv : the preprint server for biology · 2026Article
- Autoinhibitory feedback preserves intestinal stem cell maintenance and fate commitment.The EMBO journal · 2026Article
- Bipartite DNA binding domain of transcription factor BCL11B binds clustered short DNA sequence motifs.bioRxiv : the preprint server for biology · 2026Article
- The development of innate lymphoid cells.Nature immunology · 2026Review
- PLGA nanoparticles loaded with recombinant antimicrobial protein PIP significantly improves the survival state and pathological damage caused by ETEC O8-induced sepsis in mice.Frontiers in veterinary science · 2026Article
- Phantom of the immunologic opera: Unmasking the role of innate lymphoid cells (ILC) in inborn errors of immunity (IEI).Journal of human immunity · 2025Review
- The transcription factor BCL11B drives NK cell cytotoxicity and antitumor activity.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- Unlocking IL-33: New Insights into Tumor Immunity.Immune network · 2025Review
- The immunology of asthma and chronic rhinosinusitis.Nature reviews. Immunology · 2025Review
- RAG suppresses group 2 innate lymphoid cells.eLife · 2025Article
- 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
- DNA-binding affinity and specificity determine the phenotypic diversity in BCL11B-related disorders.American journal of human genetics · 2025Article
- Differential DNA methylation in infants with IgE- and non-IgE-mediated cow's milk allergy and its association with acquired tolerance.Frontiers in immunology · 2025Article
- Identification of key genes with abnormal RNA methylation modification and selected m6A regulators in ankylosing spondylitis.Immunity, inflammation and disease · 2024Article
- PU.1 and BCL11B sequentially cooperate with RUNX1 to anchor mSWI/SNF to poise the T cell effector landscape.Nature immunology · 2024Article
- The role of transcription factors in shaping regulatory T cell identity.Nature reviews. Immunology · 2023Review
- Article
- The modulation of pulmonary group 2 innate lymphoid cell function in asthma: from inflammatory mediators to environmental and metabolic factors.Experimental & molecular medicine · 2023Review
- Bcl11b sustains multipotency and restricts effector programs of intestinal-resident memory CD8Science immunology · 2023Article
- Strength of CAR signaling determines T cell versus ILC differentiation from pluripotent stem cells.Cell reports · 2023Article
47 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors at 5 institutions in 1 country.
Funding
Abstract
Type 2 innate lymphoid cells (ILC2s) promote anti-helminth responses and contribute to allergies. Here, we report that Bcl11b, previously considered a T-cell-specific transcription factor, acted directly upstream of the key ILC2 transcription factor Gfi1 to maintain its expression in mature ILC2s. Consequently, Bcl11b(-/-) ILC2s downregulated Gata3 and downstream genes, including Il1rl1 (encoding IL-33 receptor), and upregulated Rorc and type 3 ILC (ILC3) genes. Additionally, independent of Gfi1, Bcl11b directly repressed expression of the gene encoding the ILC3 transcription factor Ahr, further contributing to silencing of ILC3 genes in ILC2s. Thus, Bcl11b(-/-) ILC2s lost their functions and gained ILC3 functions, and although they expanded in response to the protease allergen papain, they produced ILC3 but not ILC2 cytokines and caused increased airway infiltration of neutrophils instead of eosinophils. Our results demonstrate that Bcl11b is more than just a T-cell-only transcription factor and establish that Bcl11b sustains mature ILC2 genetic and functional programs and lineage fidelity.
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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.