Evidence map›Paper›PMID 22876184›Full record

ArticlePLoS pathogens2012

IL-10 suppression of NK/DC crosstalk leads to poor priming of MCMV-specific CD4 T cells and prolonged MCMV persistence.

Sanja Mandaric, Senta M Walton, Thomas Rülicke, Kirsten Richter, Mathilde J H Girard-Madoux, Björn E Clausen, Antonija Zurunic, Masahito Kamanaka, Richard A Flavell, Stipan Jonjic and 1 more

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

50 citing papers in PubMed, 78 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. The natural killer cell activating receptor, NKG2D, is critical to antibody-dependent chronic rejection in heart transplantation.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2021
    Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Human Cytomegalovirus Interleukin 10 Homologs: Facing the Immune System.Frontiers in cellular and infection microbiology · 2020
    Review
  16. Review
  17. Cytomegalovirus (CMV) Pneumonitis: Cell Tropism, Inflammation, and Immunity.International journal of molecular sciences · 2019
    Review
  18. Article
  19. Article
  20. 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

11 authors at 5 institutions in 5 countries.

Sanja MandaricInstitute of Microbiology, ETH Zurich, Zurich, Switzerland.
Senta M Walton
Thomas Rülicke
Kirsten Richter
Mathilde J H Girard-Madoux
Björn E Clausen
Antonija Zurunic
Masahito Kamanaka
Richard A Flavell
Stipan Jonjic
Annette Oxenius
ETH Zurich · CHErasmus MC · NLHoward Hughes Medical Institute · USUniversity of Rijeka · HRUniversity of Veterinary Medicine Vienna · AT

Funding

Howard Hughes Medical Institute
6 · The paper itself

Abstract

IL-10 is an anti-inflammatory cytokine that regulates the extent of host immunity to infection by exerting suppressive effects on different cell types. Herpes viruses induce IL-10 to modulate the virus-host balance towards their own benefit, resulting in prolonged virus persistence. To define the cellular and molecular players involved in IL-10 modulation of herpes virus-specific immunity, we studied mouse cytomegalovirus (MCMV) infection. Here we demonstrate that IL-10 specifically curtails the MCMV-specific CD4 T cell response by suppressing the bidirectional crosstalk between NK cells and myeloid dendritic cells (DCs). In absence of IL-10, NK cells licensed DCs to effectively prime MCMV-specific CD4 T cells and we defined the pro-inflammatory cytokines IL-12, IFN-γ and TNF-α as well as NK cell activating receptors NKG2D and NCR-1 to regulate this bidirectional NK/DC interplay. Consequently, markedly enhanced priming of MCMV-specific CD4 T cells in Il10(-/-) mice led to faster control of lytic viral replication, but this came at the expense of TNF-α mediated immunopathology. Taken together, our data show that early induction of IL-10 during MCMV infection critically regulates the strength of the innate-adaptive immune cell crosstalk, thereby impacting beneficially on the ensuing virus-host balance for both the virus and the host.

Indexed as

AnimalsCD4-Positive T-LymphocytesCytokinesDendritic CellsHerpesviridae InfectionsInterleukin-10Killer Cells, NaturalMiceMice, KnockoutMuromegalovirusVirus ReplicationCytokinesIL10 protein, mouseInterleukin-10

Identifiers

PMID22876184
PMCPMC3410900
OpenAlexW2097266071

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.