Evidence map›Paper›PMID 10510336›Full record

ArticleThe Journal of clinical investigation1999

Human major group rhinoviruses downmodulate the accessory function of monocytes by inducing IL-10.

J Stöckl, H Vetr, O Majdic, G Zlabinger, E Kuechler, W Knapp

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing 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

30 citing papers in PubMed, 82 citations in OpenAlex.

  1. Trial
  2. Review
  3. Mechanism of Rhinovirus Immunity and Asthma.Frontiers in immunology · 2021
    Review
  4. Article
  5. Article
  6. Article
  7. How does rhinovirus cause the common cold cough?BMJ open respiratory research · 2016
    Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. Article
  18. Human monocytic cells direct the robust release of CXCL10 by bronchial epithelial cells during rhinovirus infection.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2010
    Article
  19. Review
  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

6 authors at 2 institutions in 2 countries.

J StöcklInstitute of Immunology, and Institute of Biochemistry, University of Vienna, A-1090 Vienna, Austria. Johannes.Stoeckle@univie.ac.at
H Vetr
O Majdic
G Zlabinger
E Kuechler
W Knapp
Institute of Immunology · HRUniversity of Vienna · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Human rhinoviruses (HRVs) are the predominant cause of the common cold. Although this disease is per se rather harmless, HRV infection is considered to set the stage for more dangerous pathogens in vivo. Here we demonstrate that HRV-14, a member of the major group HRV family, can efficiently inhibit antigen-induced T-cell proliferation and T-cell responses to allogeneic monocytes. HRV-14 triggered a significant downregulation of MHC class II molecules on monocytes. Moreover, supernatants from monocytes cultured in the presence of HRV-14 strongly reduced the allogeneic T-cell stimulatory property of untreated monocytes and monocyte-derived dendritic cells (md-DCs), whereas Epstein Barr virus-transformed B-lymphoblastoid cells were not sensitive. Analysis of the supernatant revealed that HRV-14 induced the production of significant amounts of the immunosuppressive cytokine IL-10. The important T-cell stimulatory cytokine IL-12 or the proinflammatory cytokines IL-1beta or TNF-alpha were not detected or were only minimally detected. Finally, monocytes pretreated with HRV-14 were greatly inhibited in their production of IL-12 upon stimulation with IFN-gamma/LPS. These observations suggest that altered cytokine production in mononuclear phagocytes upon interaction with HRV downmodulates appropriate immune responses during the viral infection.

Indexed as

Antigens, CDCells, CulturedEnterotoxinsGene Expression RegulationGranulocyte-Macrophage Colony-Stimulating FactorHeLa CellsHumansInterleukin-1Interleukin-10Interleukin-4KineticsLymphocyte ActivationMonocytesMuromonab-CD3Recombinant ProteinsRhinovirusAntigens, CDenterotoxin A, Staphylococcalenterotoxin B, staphylococcalEnterotoxinsGranulocyte-Macrophage Colony-Stimulating FactorInterleukin-1Interleukin-10Interleukin-4Muromonab-CD3Recombinant ProteinsTetanus ToxoidTumor Necrosis Factor-alpha

Identifiers

PMID10510336
PMCPMC408557
OpenAlexW2000798227

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.