ArticleFrontiers in immunology2013
Modulation of Signal Strength Switches Notch from an Inducer of T Cells to an Inducer of ILC2.
Article in Frontiers in immunology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
34 citing papers in PubMed.
- A human NK cell progenitor that originates in the thymus and generates KIRScience advances · 2025Article
- Thymflammation: The Role of a Constitutively Active Inflammatory Network and "Ectopic" Cell Types in the Thymus in the Induction of T Cell Tolerance and Beyond.Immunological reviews · 2025Review
- RAG suppresses group 2 innate lymphoid cells.eLife · 2025Article
- Overview of the development, characterization, and function of human types 1, 2, and 3 innate lymphoid cells.Einstein (Sao Paulo, Brazil) · 2024Review
- Strength of CAR signaling determines T cell versus ILC differentiation from pluripotent stem cells.Cell reports · 2023Article
- Transcriptional control of ILC identity.Frontiers in immunology · 2023Review
- Allergen immunotherapy combined with Notch pathway inhibitors improves HDM-induced allergic airway inflammation and inhibits ILC2 activation.Frontiers in immunology · 2023Article
- ILC Differentiation in the Thymus.Advances in experimental medicine and biology · 2022Article
- Delineating spatiotemporal and hierarchical development of human fetal innate lymphoid cells.Cell research · 2021Article
- A follicular regulatory Innate Lymphoid Cell population impairs interactions between germinal center Tfh and B cells.Communications biology · 2021Article
- The Notch signaling pathway involvement in innate lymphoid cell biology.Biomedical journal · 2021Review
- EfficientFrontiers in immunology · 2021Article
- The interplay between innate lymphoid cells and T cells.Mucosal immunology · 2020Review
- Group 2 Innate Lymphoid Cells in Human Respiratory Disorders.Journal of innate immunity · 2020Review
- Ancient Cytokine Interleukin 15-Like (IL-15L) Induces a Type 2 Immune Response.Frontiers in immunology · 2020Article
- Notch Signaling Orchestrates Helminth-Induced Type 2 Inflammation.Trends in immunology · 2019Review
- Suppression of ILC2 differentiation from committed T cell precursors by E protein transcription factors.The Journal of experimental medicine · 2019Article
- Pulmonary group 2 innate lymphoid cells: surprises and challenges.Mucosal immunology · 2019Review
- BET Bromodomain Inhibitor iBET151 Impedes Human ILC2 Activation and Prevents Experimental Allergic Lung Inflammation.Frontiers in immunology · 2019Article
- Deconstructing deployment of the innate immune lymphocyte army for barrier homeostasis and protection.Immunological reviews · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Innate lymphoid cells (ILCs) are emerging key players of the immune system with close lineage relationship to T cells. ILC2 play an important role in protective immunity against multicellular parasites, but are also involved in the pathogenesis of type 2 immune diseases. Here, we have studied the developmental requirements for human ILC2. We report that ILC2 are present in the thymus of young human donors, possibly reflecting local differentiation. Furthermore, we show that uncommitted lineage(-)CD34(+)CD1a(-)human thymic progenitors have the capacity to develop into ILC2 in vitro under the influence of Notch signaling, either by stimulation with the Notch ligand Delta like 1 (Dll1) or by expression of the active intracellular domain of NOTCH1 (NICD1). The capacity of NICD1 to mobilize the ILC2 differentiation program was sufficiently potent to override commitment to the T cell lineage in CD34(+)CD1a(+) progenitors and force them into the ILC2 lineage. As Notch is an important factor also for T cell development, these results raise the question how one and the same signaling pathway can elicit such distinct developmental outcomes from the same precursors. We provide evidence that Notch signal strength is a critical determinant in this decision: by tuning signal amplitude, Notch can be converted from a T cell inducer (low signal strength) to an ILC2 inducer (high signal strength). Thus, this study enhances our understanding of human ILC2 development and identifies a mechanism determining specificity of Notch signal output during T cell and ILC2 differentiation.
Indexed as
Identifiers
What OpenQuestion holds
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.