ArticleeLife2021
Role of the transcriptional regulator SP140 in resistance to bacterial infections via repression of type I interferons.
Open access · goldAbstract read
In one paragraph
Article in eLife, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers, 1 of them a synthesis that pooled it.
0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed, 1 pooled it
4.3field-weighted citation impact, top 4% of its field
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
71 citing papers in PubMed, 1 synthesis or guideline pooled it, 101 citations in OpenAlex.
- Clinical and mechanistic insights into the expression of SP100 family proteins in various cancers: a systematic review.BMC cancer · 2025Pooled it
- Article
- Strong, sustained type I IFN signaling acts cell intrinsically to impair IFNγ responses and cause tuberculosis susceptibility.Cell host & microbe · 2026Article
- IFN𝛾 and IFN𝛾 mimetics prevent IFN-I-mediated TB susceptibility by regulating iron metabolism and lipid peroxidation.bioRxiv : the preprint server for biology · 2026Article
- The lung tissue environment inbioRxiv : the preprint server for biology · 2026Article
- Diverse infection models demonstrate robust resistance ofbioRxiv : the preprint server for biology · 2026Article
- Cas9eLife · 2026Article
- TGFβ primes alveolar-like macrophages to induce type I IFN following TLR2 activation.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- Elimination of senescent cells with senolytic drugs as adjunctive host-directed therapy reduces tuberculosis progression in mice.Nature communications · 2026Article
- Review
- Single-cell profiling reveals that dynamic lung immune responses distinguish protection from susceptibility to tuberculosis.PLoS pathogens · 2026Article
- A Vertebrate Toxin-Antidote System That Sabotages Mouse Embryogenesis.bioRxiv : the preprint server for biology · 2026Article
- Strain-dependent disease progression and necrotizing granuloma formation in a murine model induced by virulent strains ofMicrobiology spectrum · 2026Article
- The ubiquitin ligase CBL and Fas-associated factor 2 cooperate to regulate the innate immune response to M. tuberculosis.PLoS pathogens · 2026Article
- Strong sustained type I IFN signaling acts cell intrinsically to impair IFNγ responses and cause tuberculosis susceptibility.bioRxiv : the preprint server for biology · 2026Article
- T cell-macrophage interactions in tuberculosis: What we've got here is failure to communicate.Journal of internal medicine · 2026Review
- AFrontiers in tuberculosis · 2026Article
- Pathogenicity and virulence ofVirulence · 2025Review
- Type I IFN drives neutrophil swarming, impeding lung T cell-macrophage interactions and TB control.The Journal of experimental medicine · 2025Article
- A machine learning model and molecular clusters of epigenetic chromatin regulators in tuberculosis based on bioinformatics and clinical samples.Scientific reports · 2025Article
11 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
16 authors at 6 institutions in 2 countries.
Daisy X Ji *Division of Immunology and Pathogenesis, Department of Molecular and Cell Biology, University of California, Berkeley, Berkeley, United States.ORCID 0000-0002-9148-3620
Kristen C Witt *Division of Immunology and Pathogenesis, Department of Molecular and Cell Biology, University of California, Berkeley, Berkeley, United States.ORCID 0000-0001-8744-9457
Dmitri I KotovDivision of Immunology and Pathogenesis, Department of Molecular and Cell Biology, University of California, Berkeley, Berkeley, United States.ORCID 0000-0001-7843-1503
Shally R MargolisDivision of Immunology and Pathogenesis, Department of Molecular and Cell Biology, University of California, Berkeley, Berkeley, United States.
Alexander LouieDivision of Immunology and Pathogenesis, Department of Molecular and Cell Biology, University of California, Berkeley, Berkeley, United States.
Victoria ChevéeDivision of Immunology and Pathogenesis, Department of Molecular and Cell Biology, University of California, Berkeley, Berkeley, United States.
Katherine J ChenDivision of Immunology and Pathogenesis, Department of Molecular and Cell Biology, University of California, Berkeley, Berkeley, United States.
Moritz M GaidtDivision of Immunology and Pathogenesis, Department of Molecular and Cell Biology, University of California, Berkeley, Berkeley, United States.
Harmandeep S DhaliwalCancer Research Laboratory, University of California, Berkeley, Berkeley, United States.
Angus Y LeeCancer Research Laboratory, University of California, Berkeley, Berkeley, United States.
Stephen L NishimuraDepartment of Pathology, University of California, San Francisco, San Francisco, United States.
Dario S ZamboniDepartment of Cell Biology, Ribeirão Preto Medical School, University of São Paulo, São Paulo, Brazil.ORCID 0000-0002-7856-7512
Igor KramnikThe National Emerging Infectious Diseases Laboratory, Department of Medicine (Pulmonary Center), and Department of Microbiology, Boston University School of Medicine, Boston, United States.ORCID 0000-0001-6511-9246
Daniel A PortnoyDivision of Immunology and Pathogenesis, Department of Molecular and Cell Biology, University of California, Berkeley, Berkeley, United States.
K Heran DarwinDepartment of Microbiology, New York University Grossman School of Medicine, New York, United States.
Russell E VanceDivision of Immunology and Pathogenesis, Department of Molecular and Cell Biology, University of California, Berkeley, Berkeley, United States.ORCID 0000-0002-6686-3912
University of California, Berkeley · USHoward Hughes Medical Institute · USBoston University · USNew York University · USUniversidade de São Paulo · BRUniversity of California, San Francisco · US
Funding
The role of Listeria cyclic-di-AMP during infection and immunityP01AI063302 · NIAID · UNIVERSITY OF CALIFORNIA BERKELEY · PI PORTNOY, DANIEL A · 2004 to 2025
$45.5MListeria Hemolysis and Escape From a VacuoleR01AI027655 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI DANIEL A PORTNOY · 1993 to 2026
$10.1MStructural mechanism of integrin-mediated TGF-b activationR01HL134183 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI Yifan Cheng, Stephen L Nishimura · 2016 to 2026
$5.9MNecrosis in pulmonary TB granulomas: dynamics, mechanisms, therapiesR01HL126066 · NHLBI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI KRAMNIK, IGOR, NIEDERWEIS, MICHAEL · 2016 to 2025
$5.6MFunctional and Structural Dissection of Inflammasome ActivationR37AI075039 · NIAID · UNIVERSITY OF CALIFORNIA BERKELEY · PI RUSSELL E VANCE · 2018 to 2026
$3.8MAberrant immune activation in the tuberculosis granuloma: a pivotal role in necrosisR01HL133190 · NHLBI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI BISHAI, WILLIAM RAMSES, KRAMNIK, IGOR · 2016 to 2019
$3.0MDissection of Shigella pathogenesis in vivo using a new oral infection mouse modelR01AI155634 · NIAID · UNIVERSITY OF CALIFORNIA BERKELEY · PI VANCE, RUSSELL E · 2020 to 2024
$2.2MHoward Hughes Medical InstituteNHLBI NIH HHS R01 HL126066NHLBI NIH HHS R01 HL133190NHLBI NIH HHS R01 HL134183NIAID NIH HHS P01 AI063302NIAID NIH HHS R01 AI027655NIAID NIH HHS R01 AI155634NIAID NIH HHS R37 AI075039
Abstract
Type I interferons (IFNs) are essential for anti-viral immunity, but often impair protective immune responses during bacterial infections. An important question is how type I IFNs are strongly induced during viral infections, and yet are appropriately restrained during bacterial infections. The
Indexed as
AllelesAnimalsBacterial InfectionsFemaleGene Expression RegulationInterferon Type IMacrophagesMaleMiceMice, KnockoutMinor Histocompatibility AntigensMycobacterium tuberculosisNuclear ProteinsReceptor, Interferon alpha-betaSpecific Pathogen-Free OrganismsTranscription FactorsIfnar1 protein, mouseInterferon Type IMinor Histocompatibility AntigensNuclear ProteinsReceptor, Interferon alpha-betaSp110 protein, mouseTranscription FactorsTumor Necrosis Factor-alphaimmunologyinflammationlegionella pneumophilamousemycobacterium tuberculosistype i interferon
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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.