Evidence map›Paper›PMID 27117406›Full record

ArticleCell reports2016

TNF-Mediated Restriction of Arginase 1 Expression in Myeloid Cells Triggers Type 2 NO Synthase Activity at the Site of Infection.

Ulrike Schleicher, Katrin Paduch, Andrea Debus, Stephanie Obermeyer, Till König, Jessica C Kling, Eliana Ribechini, Diana Dudziak, Dimitrios Mougiakakos, Peter J Murray and 3 more

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers.

0numbers the graph read from it
0cells of the map it votes in
76citing papers in PubMed
11.8field-weighted citation impact, top 1% of its field
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.

3 · Its place in the literature

Who cites it

76 citing papers in PubMed, 130 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. bioRxiv : the preprint server for biology · 2026
    Article
  8. Frontiers in immunology · 2026
    Review
  9. Review
  10. Article
  11. Article
  12. The roles of arginases and arginine in immunity.Nature reviews. Immunology · 2025
    Review
  13. Review
  14. Article
  15. Review
  16. The intersection of hostMicrobiology and molecular biology reviews : MMBR · 2024
    Review
  17. Article
  18. Article
  19. Article
  20. Leishmaniasis: Immune Cells Crosstalk in Macrophage Polarization.Tropical medicine and infectious disease · 2023
    Review

16 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors at 6 institutions in 3 countries.

Ulrike SchleicherMikrobiologisches Institut-Klinische Mikrobiologie, Immunologie und Hygiene, Friedrich-Alexander-Universität (FAU) Erlangen-Nürnberg and Universitätsklinikum Erlangen, 91054 Erlangen, Germany; Medical Immunology Campus Erlangen, FAU Erlangen-Nürnberg, 91054 Erlangen, Germany.
Katrin PaduchMikrobiologisches Institut-Klinische Mikrobiologie, Immunologie und Hygiene, Friedrich-Alexander-Universität (FAU) Erlangen-Nürnberg and Universitätsklinikum Erlangen, 91054 Erlangen, Germany.
Andrea DebusMikrobiologisches Institut-Klinische Mikrobiologie, Immunologie und Hygiene, Friedrich-Alexander-Universität (FAU) Erlangen-Nürnberg and Universitätsklinikum Erlangen, 91054 Erlangen, Germany.
Stephanie ObermeyerMikrobiologisches Institut-Klinische Mikrobiologie, Immunologie und Hygiene, Friedrich-Alexander-Universität (FAU) Erlangen-Nürnberg and Universitätsklinikum Erlangen, 91054 Erlangen, Germany.
Till KönigAbteilung Mikrobiologie und Hygiene, Institut für Medizinische Mikrobiologie und Hygiene, Albert-Ludwigs-Universität Freiburg, 79104 Freiburg, Germany.
Jessica C KlingMenzies Institute for Medical Research Tasmania, Hobart, Tasmania 7000, Australia.
Eliana RibechiniInstitute of Virology and Immunobiology, University of Würzburg, 97078 Würzburg, Germany.
Diana DudziakMedical Immunology Campus Erlangen, FAU Erlangen-Nürnberg, 91054 Erlangen, Germany; Laboratory of DC Biology, Department of Dermatology, FAU Erlangen-Nürnberg and Universitätsklinikum Erlangen, 91054 Erlangen, Germany.
Dimitrios MougiakakosMedical Immunology Campus Erlangen, FAU Erlangen-Nürnberg, 91054 Erlangen, Germany; Department of Internal Medicine 5, Hematology and Oncology, FAU Erlangen-Nürnberg and Universitätsklinikum Erlangen, 91054 Erlangen, Germany.
Peter J MurrayDepartments of Infectious Diseases and Immunology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA.
Renato OstuniDepartment of Experimental Oncology, European Institute of Oncology (IEO), 20139 Milan, Italy.
Heinrich KörnerMenzies Institute for Medical Research Tasmania, Hobart, Tasmania 7000, Australia.
Christian BogdanMikrobiologisches Institut-Klinische Mikrobiologie, Immunologie und Hygiene, Friedrich-Alexander-Universität (FAU) Erlangen-Nürnberg and Universitätsklinikum Erlangen, 91054 Erlangen, Germany; Medical Immunology Campus Erlangen, FAU Erlangen-Nürnberg, 91054 Erlangen, Germany. Electronic address: christian.bogdan@uk-erlangen.de.
Universitätsklinikum Erlangen · DEMenzies Institute for Medical ResearchEuropean Institute of Oncology · ITSt. Jude Children's Research Hospital · USUniversity of Freiburg · DEUniversity of Würzburg · DE

Funding

Viral Vector Technology (VVTSR)P30CA021765 · NCI · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI CHARLES ROBERTS · 1985 to 2026
$166.9M
T-CELL TARGETING FOR GVHDR01HL056067 · NHLBI · UNIVERSITY OF MINNESOTA TWIN CITIES · PI BLAZAR, BRUCE R · 1995 to 2022
$5.4M
(PQB2) Ontogeny of the tumor-immune interplay in a developmental malignancyR21CA189990 · NCI · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI MURRAY, PETER J. · 2014 to 2015
$426k
NCI NIH HHS P30 CA021765NCI NIH HHS R21 CA189990NHLBI NIH HHS R01 HL056067
6 · The paper itself

Abstract

Neutralization or deletion of tumor necrosis factor (TNF) causes loss of control of intracellular pathogens in mice and humans, but the underlying mechanisms are incompletely understood. Here, we found that TNF antagonized alternative activation of macrophages and dendritic cells by IL-4. TNF inhibited IL-4-induced arginase 1 (Arg1) expression by decreasing histone acetylation, without affecting STAT6 phosphorylation and nuclear translocation. In Leishmania major-infected C57BL/6 wild-type mice, type 2 nitric oxide (NO) synthase (NOS2) was detected in inflammatory dendritic cells or macrophages, some of which co-expressed Arg1. In TNF-deficient mice, Arg1 was hyperexpressed, causing an impaired production of NO in situ. A similar phenotype was seen in L. major-infected BALB/c mice. Arg1 deletion in hematopoietic cells protected these mice from an otherwise lethal disease, although their disease-mediating T cell response (Th2, Treg) was maintained. Thus, deletion or TNF-mediated restriction of Arg1 unleashes the production of NO by NOS2, which is critical for pathogen control.

Indexed as

AcetylationAnimalsArginaseBiomarkersCell CountDendritic CellsHistonesInterleukin-4Leishmania majorLeishmaniasisMacrophagesMice, Inbred BALB CMice, Inbred C57BLMyeloid CellsNitric OxideNitric Oxide Synthase Type II3-nitrotyrosineArginaseBiomarkersHistonesInterleukin-4Nitric OxideNitric Oxide Synthase Type IISTAT6 Transcription FactorTumor Necrosis Factor-alphaTyrosine

Identifiers

PMID27117406
PMCPMC5065922
OpenAlexW2337900869

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.