Article in Nature immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it
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.
2 · The registry
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.
Feiya OuDepartment of Pathology and Immunology, Washington University in St. Louis School of Medicine, St. Louis, MO, USA.
Tian-Tian LiuDepartment of Pathology and Immunology, Washington University in St. Louis School of Medicine, St. Louis, MO, USA.ORCID http://orcid.org/0000-0001-9377-9938
Jing ChenDepartment of Pathology and Immunology, Washington University in St. Louis School of Medicine, St. Louis, MO, USA.
Magdalena KraftDepartment of Pathology and Immunology, Washington University in St. Louis School of Medicine, St. Louis, MO, USA.ORCID http://orcid.org/0000-0002-2770-9947
Giri NamDepartment of Pathology and Immunology, Washington University in St. Louis School of Medicine, St. Louis, MO, USA.
Bishan BhattaraiDepartment of Pathology and Immunology, Washington University in St. Louis School of Medicine, St. Louis, MO, USA.ORCID http://orcid.org/0009-0003-1263-8554
Hyeyoon ShinDepartment of Pathology and Immunology, Washington University in St. Louis School of Medicine, St. Louis, MO, USA.
Alyssa R KochDepartment of Pathology and Immunology, Washington University in St. Louis School of Medicine, St. Louis, MO, USA.
Theresa L MurphyDepartment of Pathology and Immunology, Washington University in St. Louis School of Medicine, St. Louis, MO, USA.
Kenneth M MurphyDepartment of Pathology and Immunology, Washington University in St. Louis School of Medicine, St. Louis, MO, USA. kmurphy@wustl.edu.ORCID http://orcid.org/0000-0002-3505-9630
Funding
Molecular Basis of cDC1 DevelopmentR01AI162643 · NIAID · WASHINGTON UNIVERSITY · PI MURPHY, KENNETH M · 2022 to 2025
$2.8M
Function of Wdfy4 in cross-presentation and immunityR01AI150297 · NIAID · WASHINGTON UNIVERSITY · PI MURPHY, KENNETH M · 2019 to 2023
$2.5M
Understanding the Mechanisms of DC Licensing in CD8 T Cell PrimingR01CA248919 · NCI · WASHINGTON UNIVERSITY · PI MURPHY, KENNETH M · 2021 to 2025
$2.3M
Role of WDFY4 in Treg developmentR01AI191447 · NIAID · WASHINGTON UNIVERSITY · PI CHYI S HSIEH, Kenneth M Murphy · 2025 to 2026
$1.5M
Transcriptional basis of embryonic macrophage developmentR21AI163421 · NIAID · WASHINGTON UNIVERSITY · PI MURPHY, KENNETH M · 2022 to 2023
$430k
NCI NIH HHS R01 CA248919NIAID NIH HHS R01 AI150297NIAID NIH HHS R01 AI162643NIAID NIH HHS R01 AI191447NIAID NIH HHS R21 AI163421U.S. Department of Health & Human Services | NIH | National Cancer Institute (NCI) R01CA248919U.S. Department of Health & Human Services | NIH | National Institute of Allergy and Infectious Diseases (NIAID) R01AI150297U.S. Department of Health & Human Services | NIH | National Institute of Allergy and Infectious Diseases (NIAID) R01AI162643U.S. Department of Health & Human Services | NIH | National Institute of Allergy and Infectious Diseases (NIAID) R21AI163421
6 · The paper itself
Abstract
The transcriptional regulator ID2 is required for type 1 classical dendritic cell (cDC1) specification, yet the mechanism has remained obscure. We previously identified the Zeb2 -165-kb enhancer as key to normal hematopoiesis, controlled by competing CEBP and NFIL3 inputs during myeloid dendritic cell divergence. Here we uncover an unprecedented role for E proteins in myelopoiesis and demonstrate that ID2 promotes cDC1 development by antagonizing E protein activity at E-boxes within the Zeb2 enhancer. Deleting these E-boxes abolishes B cell and plasmacytoid dendritic cell development while skewing myelopoiesis toward cDC1s. Remarkably, E-box deletion rescues cDC1 development in Id2-deficient mice. These findings support a two-step model in which NFIL3 transiently represses Zeb2, followed by ID2-mediated inhibition of E proteins to stabilize cDC1 fate specification. Further, this work defines a paradigm of 'site-specific pleiotropy', wherein distinct transcription factor motifs-E-boxes and CEBP sites-within a single enhancer direct diverse cell fates.
Indexed as
CadherinsDendritic CellsEnhancer Elements, GeneticInhibitor of Differentiation Protein 2Zinc Finger E-box Binding Homeobox 2AnimalsBasic-Leucine Zipper Transcription FactorsCCAAT-Enhancer-Binding ProteinsCell DifferentiationEnhancer of Zeste Homolog 2 ProteinHematopoiesisMiceMice, KnockoutBasic-Leucine Zipper Transcription FactorsCadherinsCCAAT-Enhancer-Binding ProteinsEnhancer of Zeste Homolog 2 ProteinIdb2 protein, mouseInhibitor of Differentiation Protein 2Nfil3 protein, mouseZEB2 protein, mouseZinc Finger E-box Binding Homeobox 2
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.
ID2 secures cDC1 specification by antagonizing E proteins at a pleiotropic Zeb2 enhancer. · full record | OpenQuestion