Evidence map›Paper›PMID 24956596›Full record

ArticleMicrobes and infection2014

Herpes virus entry mediator (HVEM) modulates proliferation and activation of regulatory T cells following HSV-1 infection.

Shalini Sharma, Naveen K Rajasagi, Tamara Veiga-Parga, Barry T Rouse

Open access · greenAbstract read
In one paragraph

Article in Microbes and infection, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

17 citing papers in PubMed, 24 citations in OpenAlex.

  1. Review
  2. Herpes Simplex Virus Type 1 Interactions with the Interferon System.International journal of molecular sciences · 2020
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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 2 institutions in 1 country.

Shalini SharmaDepartment of Biomedical and Diagnostic Sciences, College of Veterinary Medicine, University of Tennessee, Knoxville, TN 37996, USA.
Naveen K RajasagiDepartment of Biomedical and Diagnostic Sciences, College of Veterinary Medicine, University of Tennessee, Knoxville, TN 37996, USA.
Tamara Veiga-PargaDepartment of Biomedical and Diagnostic Sciences, College of Veterinary Medicine, University of Tennessee, Knoxville, TN 37996, USA.
Barry T RouseDepartment of Biomedical and Diagnostic Sciences, College of Veterinary Medicine, University of Tennessee, Knoxville, TN 37996, USA. Electronic address: btr@utk.edu.
University of Tennessee at Knoxville · USKnoxville College · US

Funding

Mechanisms of Herpetic KeratitisR01EY005093 · NEI · UNIVERSITY OF TENNESSEE KNOXVILLE · PI ROUSE, BARRY T. · 1985 to 2020
$7.8M
T regulatory Cells in HSV Immunity and ImmunopathologyR01AI063365 · NIAID · UNIVERSITY OF TENNESSEE KNOXVILLE · PI ROUSE, BARRY T. · 2006 to 2015
$3.5M
NEI NIH HHS EY 005093NEI NIH HHS R01 EY005093NIAID NIH HHS AI 063365NIAID NIH HHS R01 AI063365
6 · The paper itself

Abstract

In many infections, especially those that are chronic such as Herpes Simplex Virus-1 (HSV-1), the outcome may be influenced by the activity of one or more types of regulatory T cells (Tregs). Some infections can cause Treg expansion, but how viruses might promote preferential Treg expansion is has been unclear. In this report, we demonstrate a possible mechanism by which HSV (Herpes Simplex virus-1) infection could act to signal and expands the Treg population. We show that CD4(+) FoxP3(+) Tregs up- regulate HVEM (herpes virus entry mediator), which is a binding site for major viral glycoprotein HSVgD, following HSV infection, which is a binding site for major viral glycoprotein HSVgD. Recombinant HSVgD enhanced the proliferation of CD4(+) FoxP3(+) Tregs cells in-vitro. Furthermore, compared to wild type (WT), HVEM deficient mice (HVEM-/-) generated a weaker Treg responses represented by significantly diminished ratios of CD4(+)FoxP3(+)/CD4(+)FoxP3(-) cells along with diminished proportions of FoxP3(+) Tregscells co-expressing Treg activation markers and a reduced MFI of FoxP3 expression on CD4(+) T cells. Consistent with defective Treg responses, HVEM-/- animals were more susceptible to HSV-1 induced ocular immunopathology, with more severe lesions in HVEM-/- animals. Our results indicate that HVEM regulates Treg responses, and its modulation could represent a useful approach to control HSV induced corneal immunopathology.

Indexed as

Cell ProliferationLymphocyte ActivationAnimalsDisease Models, AnimalFemaleHerpesvirus 1, HumanKeratitis, HerpeticMice, Inbred C57BLMice, KnockoutReceptors, Tumor Necrosis Factor, Member 14Receptors, VirusT-Lymphocytes, RegulatoryVirus InternalizationReceptors, Tumor Necrosis Factor, Member 14Receptors, VirusTnfrsf14 protein, mousegDHSKHSV-1HVEMTregs

Identifiers

PMID24956596
PMCPMC4150749
OpenAlexW2054927389

What OpenQuestion holds

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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.