Evidence map›Paper›PMID 22021615›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2011

Influence of galectin-9/Tim-3 interaction on herpes simplex virus-1 latency.

Pradeep B J Reddy, Sharvan Sehrawat, Amol Suryawanshi, Naveen K Rajasagi, Sachin Mulik, Mitsuomi Hirashima, Barry T Rouse

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed, 1 pooled it
2.2field-weighted citation impact, top 13% 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

41 citing papers in PubMed, 1 synthesis or guideline pooled it, 58 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Article
  6. Galectin-9: diverse roles in skin disease.Frontiers in allergy · 2025
    Review
  7. Review
  8. Myeloid-Derived Suppressor Cells Induce Exhaustion-Like CD8International journal of biological sciences · 2024
    Article
  9. The role of galectins in immunity and infection.Nature reviews. Immunology · 2023
    Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Herpesviruses: Harmonious Pathogens but Relevant Cofactors in Other Diseases?Frontiers in cellular and infection microbiology · 2018
    Review
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

7 authors at 4 institutions in 2 countries.

Pradeep B J ReddyDepartment of Pathobiology, College of Veterinary Medicine, University of Tennessee, Knoxville, TN 37996, USA.
Sharvan Sehrawat
Amol Suryawanshi
Naveen K Rajasagi
Sachin Mulik
Mitsuomi Hirashima
Barry T Rouse
Knoxville College · USKagawa University · JPUniversity of Tennessee at Knoxville · USWhitehead Institute for Biomedical Research · 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

After HSV-1 infection, CD8(+) T cells accumulate in the trigeminal ganglion (TG) and participate in the maintenance of latency. However, the mechanisms underlying intermittent virus reactivation are poorly understood. In this study, we demonstrate the role of an inhibitory interaction between T cell Ig and mucin domain-containing molecule 3 (Tim-3)-expressing CD8(+) T cells and galectin 9 (Gal-9) that could influence HSV-1 latency and reactivation. Accordingly, we show that most K(b)-gB tetramer-specific CD8(+) T cells in the TG of HSV-1-infected mice express Tim-3, a molecule that delivers negative signals to CD8(+) T cells upon engagement of its ligand Gal-9. Gal-9 was also upregulated in the TG when replicating virus was present as well during latency. This could set the stage for Gal-9/Tim-3 interaction, and this inhibitory interaction was responsible for reduced CD8(+) T cell effector function in wild-type mice. Additionally, TG cell cultures exposed to recombinant Gal-9 in the latent phase caused apoptosis of most CD8(+) T cells. Furthermore, Gal-9 knockout TG cultures showed delayed and reduced viral reactivation as compared with wild-type cultures, demonstrating the greater efficiency of CD8(+) T cells to inhibit virus reactivation in the absence of Gal-9. Moreover, the addition of recombinant Gal-9 to ex vivo TG cultures induced enhanced viral reactivation compared with untreated controls. Our results demonstrate that the host homeostatic mechanism mediated by Gal-9/Tim-3 interaction on CD8(+) T cells can influence the outcome of HSV-1 latent infection, and manipulating Gal-9 signals might represent therapeutic means to inhibit HSV-1 reactivation from latency.

Indexed as

AnimalsApoptosisBlotting, WesternCD8-Positive T-LymphocytesCell SeparationFemaleFlow CytometryFluorescent Antibody TechniqueGalectinsHepatitis A Virus Cellular Receptor 2Herpes SimplexMiceMice, Inbred C57BLMice, KnockoutReal-Time Polymerase Chain ReactionReceptors, Virusgalectin 9, mouseGalectinsHavcr2 protein, mouseHepatitis A Virus Cellular Receptor 2Receptors, Virus

Identifiers

PMID22021615
PMCPMC3221893
OpenAlexW1949498377

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.