Evidence map›Paper›PMID 26467188›Full record

ArticleJournal of leukocyte biology2016

Lack of the programmed death-1 receptor renders host susceptible to enteric microbial infection through impairing the production of the mucosal natural killer cell effector molecules.

Shahram Solaymani-Mohammadi, Omar Lakhdari, Ivelina Minev, Steve Shenouda, Blake F Frey, Rolf Billeskov, Steven M Singer, Jay A Berzofsky, Lars Eckmann, Martin F Kagnoff

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of leukocyte biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.0field-weighted citation impact, top 24% 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

17 citing papers in PubMed, 24 citations in OpenAlex.

  1. Trial
  2. Review
  3. Review
  4. Review
  5. Article
  6. Article
  7. Review
  8. Review
  9. Review
  10. Review
  11. Hyperprogression: A novel response pattern under immunotherapy.Clinical and translational medicine · 2020
    Review
  12. Observational
  13. Article
  14. The Outer Membrane Vesicles ofFrontiers in microbiology · 2018
    Article
  15. Article
  16. Review
  17. Article
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

10 authors at 4 institutions in 1 country.

Shahram Solaymani-Mohammadi*Laboratory of Mucosal Immunology and Department of Medicine, University of California, San Diego, La Jolla, California, USA; Vaccine Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA; and Department of Biology and Center for Infectious Disease, Georgetown University, Washington, District of Columbia, USA shahram.sm@nih.gov.
Omar Lakhdari*Laboratory of Mucosal Immunology and Department of Medicine, University of California, San Diego, La Jolla, California, USA; Vaccine Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA; and Department of Biology and Center for Infectious Disease, Georgetown University, Washington, District of Columbia, USA.
Ivelina Minev*Laboratory of Mucosal Immunology and Department of Medicine, University of California, San Diego, La Jolla, California, USA; Vaccine Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA; and Department of Biology and Center for Infectious Disease, Georgetown University, Washington, District of Columbia, USA.
Steve Shenouda*Laboratory of Mucosal Immunology and Department of Medicine, University of California, San Diego, La Jolla, California, USA; Vaccine Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA; and Department of Biology and Center for Infectious Disease, Georgetown University, Washington, District of Columbia, USA.
Blake F Frey*Laboratory of Mucosal Immunology and Department of Medicine, University of California, San Diego, La Jolla, California, USA; Vaccine Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA; and Department of Biology and Center for Infectious Disease, Georgetown University, Washington, District of Columbia, USA.
Rolf Billeskov*Laboratory of Mucosal Immunology and Department of Medicine, University of California, San Diego, La Jolla, California, USA; Vaccine Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA; and Department of Biology and Center for Infectious Disease, Georgetown University, Washington, District of Columbia, USA.
Steven M Singer*Laboratory of Mucosal Immunology and Department of Medicine, University of California, San Diego, La Jolla, California, USA; Vaccine Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA; and Department of Biology and Center for Infectious Disease, Georgetown University, Washington, District of Columbia, USA.
Jay A Berzofsky*Laboratory of Mucosal Immunology and Department of Medicine, University of California, San Diego, La Jolla, California, USA; Vaccine Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA; and Department of Biology and Center for Infectious Disease, Georgetown University, Washington, District of Columbia, USA.
Lars Eckmann*Laboratory of Mucosal Immunology and Department of Medicine, University of California, San Diego, La Jolla, California, USA; Vaccine Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA; and Department of Biology and Center for Infectious Disease, Georgetown University, Washington, District of Columbia, USA.
Martin F Kagnoff*Laboratory of Mucosal Immunology and Department of Medicine, University of California, San Diego, La Jolla, California, USA; Vaccine Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA; and Department of Biology and Center for Infectious Disease, Georgetown University, Washington, District of Columbia, USA.
Center for Cancer Research · USNational Cancer Institute · USGeorgetown University · USUniversity of California, San Diego · US

Funding

Vaccine and immunotherapy strategies for cancer and viruses causing cancerZIASC004020 · NCI · DIVISION OF CLINICAL SCIENCES - NCI · PI BERZOFSKY, JAY A · 2009 to 2025
$51.8M
TL MOLECULES AND GAMMA-DELTA T CELLSP01DK035108 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI KAGNOFF, MARTIN FREDERICK · 1986 to 2013
$19.2M
The Role of Macrophages in Immune Responses to GiardiaR15AI109591 · NIAID · GEORGETOWN UNIVERSITY · PI SINGER, STEVEN M · 2014 to 2023
$1.5M
Immune Control of Giardia PathogenesisR15AI094492 · NIAID · GEORGETOWN UNIVERSITY · PI SINGER, STEVEN M · 2011 to 2011
$461k
Intramural NIH HHSNIAID NIH HHS AI 094492NIAID NIH HHS R15 AI094492NIAID NIH HHS R15 AI109591NIDDK NIH HHS DK35108NIDDK NIH HHS P01 DK035108PHS HHS Z01-C04020
6 · The paper itself

Abstract

The programmed death-1 receptor is expressed on a wide range of immune effector cells, including T cells, natural killer T cells, dendritic cells, macrophages, and natural killer cells. In malignancies and chronic viral infections, increased expression of programmed death-1 by T cells is generally associated with a poor prognosis. However, its role in early host microbial defense at the intestinal mucosa is not well understood. We report that programmed death-1 expression is increased on conventional natural killer cells but not on CD4(+), CD8(+) or natural killer T cells, or CD11b(+) or CD11c(+) macrophages or dendritic cells after infection with the mouse pathogen Citrobacter rodentium. Mice genetically deficient in programmed death-1 or treated with anti-programmed death-1 antibody were more susceptible to acute enteric and systemic infection with Citrobacter rodentium. Wild-type but not programmed death-1-deficient mice infected with Citrobacter rodentium showed significantly increased expression of the conventional mucosal NK cell effector molecules granzyme B and perforin. In contrast, natural killer cells from programmed death-1-deficient mice had impaired expression of those mediators. Consistent with programmed death-1 being important for intracellular expression of natural killer cell effector molecules, mice depleted of natural killer cells and perforin-deficient mice manifested increased susceptibility to acute enteric infection with Citrobacter rodentium. Our findings suggest that increased programmed death-1 signaling pathway expression by conventional natural killer cells promotes host protection at the intestinal mucosa during acute infection with a bacterial gut pathogen by enhancing the expression and production of important effectors of natural killer cell function.

Indexed as

Citrobacter rodentiumAnimalsColonEnterobacteriaceae InfectionsFemaleGranzymesInterferon-gammaIntestinal MucosaKiller Cells, NaturalMaleMiceMice, Inbred C57BLPerforinProgrammed Cell Death 1 ReceptorSignal TransductionGranzymesGzmb protein, mouseInterferon-gammaPerforinProgrammed Cell Death 1 Receptorattaching/effacing bacteriaCitrobacter rodentiumgranzyme BPD-1perforin

Identifiers

PMID26467188
PMCPMC6608046
OpenAlexW2216639295

What OpenQuestion holds

Textmetadata
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.