Evidence map›Paper›PMID 34314390›Full record

ArticleThe Journal of clinical investigation2021

Natural killer cell immunosuppressive function requires CXCR3-dependent redistribution within lymphoid tissues.

Ayad Ali, Laura M Canaday, H Alex Feldman, Hilal Cevik, Michael T Moran, Sanjeeth Rajaram, Nora Lakes, Jasmine A Tuazon, Harsha Seelamneni, Durga Krishnamurthy and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

35 citing papers in PubMed, 44 citations in OpenAlex.

  1. Article
  2. Review
  3. Unconventional functions of natural killer cells in homeostasis and disease.Journal of immunology (Baltimore, Md. : 1950) · 2026
    Review
  4. Article
  5. HIV controllers, lessons learnt from the lymphoid tissues.Current opinion in HIV and AIDS · 2026
    Review
  6. Review
  7. Review
  8. CXCL10-induced chemotaxis ofMolecular therapy. Oncology · 2025
    Article
  9. Genetic Deletion of the Purinergic ReceptorACS pharmacology & translational science · 2025
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. CD56Frontiers in immunology · 2024
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

13 authors at 3 institutions in 1 country.

Ayad AliMedical Scientist Training Program and.
Laura M CanadayImmunology Graduate Training Program, University of Cincinnati College of Medicine, Cincinnati, Ohio, USA.
H Alex FeldmanMedical Scientist Training Program and.
Hilal CevikCenter for Autoimmune Genomics and Etiology, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio, USA.
Michael T MoranImmunology Graduate Training Program, University of Cincinnati College of Medicine, Cincinnati, Ohio, USA.
Sanjeeth RajaramCenter for Autoimmune Genomics and Etiology, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio, USA.
Nora LakesMedical Scientist Training Program and.
Jasmine A TuazonCenter for Autoimmune Genomics and Etiology, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio, USA.
Harsha SeelamneniCenter for Autoimmune Genomics and Etiology, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio, USA.
Durga KrishnamurthyCenter for Autoimmune Genomics and Etiology, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio, USA.
Eryn BlassCenter for Virology and Vaccine Research, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA.
Dan H BarouchCenter for Virology and Vaccine Research, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA.
Stephen N WaggonerMedical Scientist Training Program and.
Cincinnati Children's Hospital Medical Center · USBeth Israel Deaconess Medical Center · USNational Student Clearinghouse Research Center · US

Funding

Stem Cell/Organoid and Genome Editing CoreP30DK078392 · NIDDK · CINCINNATI CHILDRENS HOSP MED CTR · PI Alexander Miethke · 2007 to 2026
$24.4M
Tissue Repository CoreP30AR070549 · NIAMS · CINCINNATI CHILDRENS HOSP MED CTR · PI Leah Claire Kottyan · 2016 to 2026
$7.7M
Medical Scientist Training ProgramT32GM063483 · NIGMS · UNIVERSITY OF CINCINNATI · PI KHURANA HERSHEY, GURJIT K. · 2002 to 2022
$6.7M
A revolutionary vaccine approach to prevent HIV infection in substance abuseDP1DA038017 · NIDA · CINCINNATI CHILDRENS HOSP MED CTR · PI WAGGONER, STEPHEN N. · 2014 to 2018
$3.9M
Genomics of Inflammatory Bowel DiseaseR01AI148276 · NIAID · CINCINNATI CHILDRENS HOSP MED CTR · PI KOTTYAN, LEAH CLAIRE · 2019 to 2023
$3.9M
Targeting natural killer cells to enhance HIV vaccine responsesR01AI148080 · NIAID · CINCINNATI CHILDRENS HOSP MED CTR · PI WAGGONER, STEPHEN N. · 2019 to 2023
$3.3M
Transcription Factor Genetics in LupusR01AR073228 · NIAMS · CINCINNATI CHILDRENS HOSP MED CTR · PI KOTTYAN, LEAH CLAIRE, WAGGONER, STEPHEN N. · 2019 to 2023
$2.2M
Pathogenesis and therapeutic targeting of immune disordersT32AI118697 · NIAID · CINCINNATI CHILDRENS HOSP MED CTR · PI HILDEMAN, DAVID A · 2016 to 2020
$683k
NIAID NIH HHS R01 AI148080NIAID NIH HHS R01 AI148276NIAID NIH HHS T32 AI118697NIAMS NIH HHS P30 AR070549NIAMS NIH HHS R01 AR073228NIDA NIH HHS DP1 DA038017NIDDK NIH HHS P30 DK078392NIGMS NIH HHS T32 GM063483
6 · The paper itself

Abstract

NK cell suppression of T cells is a key determinant of viral pathogenesis and vaccine efficacy. This process involves perforin-dependent elimination of activated CD4+ T cells during the first 3 days of infection. Although this mechanism requires cell-cell contact, NK cells and T cells typically reside in different compartments of lymphoid tissues at steady state. Here, we showed that NK cell suppression of T cells is associated with transient accumulation of NK cells within T cell-rich sites of the spleen during lymphocytic choriomeningitis virus infection. The chemokine receptor CXCR3 was required for this relocation and suppression of antiviral T cells. Accordingly, NK cell migration was mediated by type I IFN-dependent promotion of CXCR3 ligand expression. In contrast, adenoviral vectors that weakly induced type I IFN and did not stimulate NK cell inhibition of T cells also did not promote measurable redistribution of NK cells to T cell zones. Exogenous IFN rescued NK cell migration during adenoviral vector immunization. Thus, type I IFN and CXCR3 were critical for properly positioning NK cells to constrain antiviral T cell responses. Development of strategies to curtail migration of NK cells between lymphoid compartments may enhance vaccine-elicited immune responses.

Indexed as

AnimalsCell MovementHost Microbial InteractionsImmune ToleranceImmunity, InnateKiller Cells, NaturalLymphocyte ActivationLymphocytic ChoriomeningitisLymphocytic choriomeningitis virusLymphoid TissueMiceMice, Inbred C57BLMice, KnockoutReceptors, CXCR3T-LymphocytesCxcr3 protein, mouseReceptors, CXCR3Cellular immune responseImmunologyInnate immunityNK cellsVaccines

Identifiers

PMID34314390
PMCPMC8439606
OpenAlexW3186528611

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.