Evidence map›Paper›PMID 25468565›Full record

ArticleImmunobiology2015

Batf3 deficiency is not critical for the generation of CD8α⁺ dendritic cells.

Kevin R Mott, Hadi Maazi, Sariah J Allen, Mandana Zandian, Harry Matundan, Yasamin N Ghiasi, Behrooz G Sharifi, David Underhill, Omid Akbari, Homayon Ghiasi

Open access · greenAbstract read
In one paragraph

Article in Immunobiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.5field-weighted citation impact, top 34% 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

13 citing papers in PubMed, 14 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. LangerinFrontiers in immunology · 2019
    Review
  10. LangerinFrontiers in immunology · 2018
    Article
  11. Article
  12. Batf3 selectively determines acquisition of CD8Immunology and cell biology · 2017
    Article
  13. 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 2 institutions in 1 country.

Kevin R MottCenter for Neurobiology and Vaccine Development, Ophthalmology Research, Department of Surgery, Cedars-Sinai Medical Center, Los Angeles, CA, USA.
Hadi MaaziDepartment of Molecular Microbiology and Immunology, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA.
Sariah J AllenCenter for Neurobiology and Vaccine Development, Ophthalmology Research, Department of Surgery, Cedars-Sinai Medical Center, Los Angeles, CA, USA.
Mandana ZandianCenter for Neurobiology and Vaccine Development, Ophthalmology Research, Department of Surgery, Cedars-Sinai Medical Center, Los Angeles, CA, USA.
Harry MatundanCenter for Neurobiology and Vaccine Development, Ophthalmology Research, Department of Surgery, Cedars-Sinai Medical Center, Los Angeles, CA, USA.
Yasamin N GhiasiDepartment of Molecular Microbiology and Immunology, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA.
Behrooz G SharifiDivision of Cardiology, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, CA, USA.
David UnderhillInflammatory Bowel & Immunobiology Research Institute, Cedars-Sinai Medical Center, Los Angeles, CA, USA.
Omid AkbariDepartment of Molecular Microbiology and Immunology, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA.
Homayon GhiasiCenter for Neurobiology and Vaccine Development, Ophthalmology Research, Department of Surgery, Cedars-Sinai Medical Center, Los Angeles, CA, USA. Electronic address: ghiasih@cshs.org.
Cedars-Sinai Medical Center · USUniversity of Southern California · US

Funding

The Role of gK in HSV-1 Induced Corneal ScarringR01EY013615 · NEI · CEDARS-SINAI MEDICAL CENTER · PI HOMAYON GHIASI · 2002 to 2026
$7.8M
Role of lymphoid DCs in HSV-1 latencyR21AI093941 · NIAID · CEDARS-SINAI MEDICAL CENTER · PI GHIASI, HOMAYON · 2012 to 2013
$439k
NEI NIH HHS EY13615NEI NIH HHS R01 EY013615NIAID NIH HHS AI093941NIAID NIH HHS R21 AI093941
6 · The paper itself

Abstract

Recently, we have reported that CD8α(+) DCs, rather than CD8(+) T cells, are involved in the establishment and maintenance of HSV-1 latency in the trigeminal ganglia (TG) of ocularly infected mice. In the current study, we investigated whether similar results can be obtained using Batf3(-/-) mice that previously were reported to lack CD8α(+) DCs. However, our results demonstrate that Batf3(-/-) mice, without any known infection, express CD8α(+) DCs. Consequently, due to the presence of CD8α(+) DCs, no differences were detected in the level of HSV-1 latency between Batf3(-/-) mice compared with wild type control mice.

Indexed as

AnimalsBasic-Leucine Zipper Transcription FactorsCD8 AntigensDendritic CellsDisease Models, AnimalGene Knockout TechniquesHerpes SimplexHerpesvirus 1, HumanImmunohistochemistryImmunophenotypingMiceMice, KnockoutPhenotypeRabbitsRepressor ProteinsBasic-Leucine Zipper Transcription FactorsCD8 antigen, alpha chainCD8 AntigensRepressor ProteinsSNFT protein, mouseCompensationDendritic cellsHSV-1KnockoutLatency

Identifiers

PMID25468565
PMCPMC4355210
OpenAlexW2080206577

What OpenQuestion holds

Textmetadata
LicenceTDM
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.