Evidence map›Paper›PMID 18815300›Full record

ArticleJournal of virology2008

Vesicular stomatitis virus matrix protein impairs CD1d-mediated antigen presentation through activation of the p38 MAPK pathway.

Gourapura J Renukaradhya, Masood A Khan, Daniel Shaji, Randy R Brutkiewicz

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

24 citing papers in PubMed, 31 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Article
  6. Immune evasion of the CD1d/NKT cell axis.Current opinion in immunology · 2018
    Review
  7. Cell Signaling Pathways That Regulate Antigen Presentation.Journal of immunology (Baltimore, Md. : 1950) · 2016
    Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Lipid antigens in immunity.Biological chemistry · 2014
    Review
  15. Article
  16. Article
  17. Article
  18. 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

4 authors at 3 institutions in 1 country.

Gourapura J RenukaradhyaDepartment of Microbiology and Immunology, Indiana University School of Medicine, Walther Oncology Center, Indianapolis, IN 46202-5181, USA.
Masood A Khan
Daniel Shaji
Randy R Brutkiewicz
Indiana University – Purdue University Indianapolis · USIndiana University School of MedicineWalther Cancer Foundation · US

Funding

Poxvirus Modulation of Immune ResponsesP01AI056097 · NIAID · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI BLUM, JANICE S · 2003 to 2010
$9.9M
REGULATION OF HEMATOPOIETIC CELL PRODUCTIONT32DK007519 · NIDDK · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI KAPLAN, MARK H · 1986 to 2020
$7.1M
CDI Molecules &NKT Cells in Host DefenseR01AI046455 · NIAID · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI BRUTKIEWICZ, RANDY R · 2000 to 2009
$2.8M
NIAID NIH HHS P01 AI056097NIAID NIH HHS P0I AI056097NIAID NIH HHS R01 AI046455NIAID NIH HHS R01 AI46455NIDDK NIH HHS T32 DK007519
6 · The paper itself

Abstract

Natural killer T (NKT) cells are unique T lymphocytes that recognize CD1d-bound lipid antigens and play an important role in both innate and acquired immune responses against infectious diseases and tumors. We have already shown that a vesicular stomatitis virus (VSV) infection results in the rapid inhibition of murine CD1d-mediated antigen presentation to NKT cells. In the present study, it was found that the VSV matrix (VSV-M) protein is an important element in this decrease in antigen presentation postinfection. The VSV-M protein altered the intracellular distribution of murine CD1d molecules, resulting in qualitative (but not quantitative) changes in cell surface CD1d expression. The M protein was distributed throughout the infected cell, and it was found to activate the mitogen-activated protein kinase (MAPK) p38 very early postinfection. Infection of CD1d(+) cells with a temperature-sensitive VSV-M mutant at the nonpermissive temperature both substantially reversed the inhibition of antigen presentation by CD1d and delayed the activation of p38. Thus, the VSV-M protein plays an important role in permitting the virus to evade important components of the innate immune response by regulating specific MAPK pathways.

Indexed as

MAP Kinase Signaling SystemAnimalsAntigen PresentationAntigens, CD1dCell LineEnzyme ActivationMicep38 Mitogen-Activated Protein KinasesProtein TransportVesiculovirusViral Matrix ProteinsAntigens, CD1dp38 Mitogen-Activated Protein KinasesViral Matrix Proteins

Identifiers

PMID18815300
PMCPMC2593331
OpenAlexW2118937284

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.