ArticleThe Journal of experimental medicine2020
c-Maf regulates the plasticity of group 3 innate lymphoid cells by restraining the type 1 program.
Article in The Journal of experimental medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 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
47 citing papers in PubMed, 73 citations in OpenAlex.
- Understanding the Variability of Peanut-Oral Immunotherapy Responses by Multi-Omics Profiling of Immune Cells.Allergy · 2025Trial
- A temporal differentiation program after birth delineates γδ T cell immunity.Science advances · 2026Article
- Enhancer hubs govern chromatin topology and Th17 cell identity.bioRxiv : the preprint server for biology · 2026Article
- Single-cell analysis of recruited ILC2 cell fate during transition from circulation to establishment of tissue residency.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- Gasdermins against intracellular bacterial pathogens.Nature microbiology · 2026Review
- The conserved noncoding sequence CNS11 is a master control region forScience advances · 2026Article
- RORγtNature communications · 2026Article
- ILC plasticity in intestinal immune barrier remodeling: current evidence and therapeutic implications for inflammatory bowel disease.Frontiers in immunology · 2026Review
- Single-cell multiomics identifies Tcf1 and Lef1 as key initiators of early thymic progenitor fate.Science immunology · 2025Article
- Circadian circuits control plasticity of group 3 innate lymphoid cells by sustaining epigenetic configuration of RORγt.Nature immunology · 2025Article
- Restriction of innate Tγδ17 cell plasticity by an AP-1 regulatory axis.Nature immunology · 2025Article
- Decoding innate lymphoid cells and innate-like lymphocytes in asthma: pathways to mechanisms and therapies.Journal of biomedical science · 2025Review
- A membrane lipid signature unravels the dynamic landscape of group 1 innate lymphoid cells across the health-disease continuum.iScience · 2025Article
- Tissue-Specific Metabolic Reprogramming in Innate Lymphoid Cells and Its Impact on Disease.Immune network · 2025Review
- Deciphering the Role of Innate Lymphoid Cells Group 3 in the Gut Microenvironment: A Narrative Review of Their Novel Contributions to Autoimmune Disease Pathogenesis.Journal of inflammation research · 2025Review
- Transcription factor c-Maf: a checkpoint that programs autoimmunity.Frontiers in immunology · 2025Review
- Restriction of innate Tγδ17 cell plasticity by an AP-1 regulatory axis.bioRxiv : the preprint server for biology · 2024Article
- Maf expression in B cells restricts reactive plasmablast and germinal center B cell expansion.Nature communications · 2024Article
- Group 1 ILCs: Heterogeneity, plasticity, and transcriptional regulation.Immunological reviews · 2024Review
- The cIAP ubiquitin ligases sustain type 3 γδ T cells and ILC during aging to promote barrier immunity.The Journal of experimental medicine · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
CCR6- group 3 innate lymphoid cells (ILC3s) are mediators of intestinal immunity and barrier function that possess the capacity to acquire type 1 effector features and fully convert into ILC1s. The molecular mechanisms governing such plasticity are undefined. Here, we identified c-Maf as an essential regulator of ILC3 homeostasis and plasticity that limits physiological ILC1 conversion. Phenotypic analysis of effector status in Maf-deficient CCR6- ILC3s, coupled with evaluation of global changes in transcriptome, chromatin accessibility, and transcription factor motif enrichment, revealed that c-Maf enforces ILC3 identity. c-Maf promoted ILC3 accessibility and supported RORγt activity and expression of type 3 effector genes. Conversely, c-Maf antagonized type 1 programming, largely through restraint of T-bet expression and function. Mapping of the dynamic changes in chromatin landscape accompanying CCR6- ILC3 development and ILC1 conversion solidified c-Maf as a gatekeeper of type 1 regulatory transformation and a controller of ILC3 fate.
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.