Evidence map›Paper›PMID 16622014›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2006

Enhancement of LFA-1-mediated T cell adhesion by human T lymphotropic virus type 1 p12I1.

Seung-Jae Kim, Amrithraj M Nair, Soledad Fernandez, Lawrence Mathes, Michael D Lairmore

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
2.1field-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

38 citing papers in PubMed, 59 citations in OpenAlex.

  1. Trial
  2. Article
  3. Complete Rescue of HTLV-1Pathogens (Basel, Switzerland) · 2024
    Article
  4. The helicase-like transcription factor redirects the autophagic flux and restricts human T cell leukemia virus type 1 infection.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Expression of TSLC1 in patients with HAM/TSP.Journal of neurovirology · 2020
    Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
  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

5 authors at 1 institution in 1 country.

Seung-Jae KimCenter for Retrovirus Research and Department of Veterinary Biosciences, Ohio State University, 1925 Coffey Road, Columbus, OH 43210, USA.
Amrithraj M Nair
Soledad Fernandez
Lawrence Mathes
Michael D Lairmore
The Ohio State University Comprehensive Cancer Center – Arthur G. James Cancer Hospital and Richard J. Solove Research Institute · US

Funding

Role of Inflammation in Tax-mediated TumorigenesisP01CA100730 · NCI · WASHINGTON UNIVERSITY · PI Malachi Griffith · 2003 to 2026
$44.8M
ANIMAL MODELS OF MOLECULAR PATHOGENSIS OF HTLV-1R01RR014324 · NCRR · OHIO STATE UNIVERSITY · PI LAIRMORE, MICHAEL D · 1999 to 2003
$1.2M
NCI NIH HHS CA 100730NCI NIH HHS CA 70529NCI NIH HHS P01 CA100730NCRR NIH HHS R01 RR014324NCRR NIH HHS RR 14324
6 · The paper itself

Abstract

Cell-to-cell transmission of retroviruses, such as human T lymphotropic virus type 1 (HTLV-1), is well documented, but the roles of viral regulatory or other nonstructural proteins in the modulation of T cell adhesion are incompletely understood. In this study we tested the role of the HTLV-1 accessory protein, p12(I), on LFA-1-mediated cell adhesion. p12(I) is critical for early HTLV-1 infection by causing the release of calcium from the endoplasmic reticulum to activate NFAT-mediated transcription. We tested the role of this novel viral protein in mediating LFA-1-dependent cell adhesion. Our data indicated that T cells expressing a mutant HTLV-1 provirus that does not produce p12(I) mRNA (ACH.p12(I)) exhibited reduced LFA-1-mediated adhesion compared with wild-type HTLV-1-expressing cells (ACH). Furthermore, the expression of p12(I) in Jurkat T cells using lentiviral vectors enhanced LFA-1-mediated cell adhesion, which was inhibited by the calcium chelator BAPTA-AM, the calcium channel blocker SK&F 96365, and calpeptin, an inhibitor of the calcium-dependent protease calpain. Similar to the intracellular calcium mobilizer, thapsigargin, the expression of p12(I) in Jurkat T cells induced cell surface clustering of LFA-1 without changing the level of integrin expression. Our data are the first to indicate that HTLV-1 p12(I), in addition to enhancing T cell activation, promotes cell-to-cell spread by inducing LFA-1 clustering on T cells via calcium-dependent signaling.

Indexed as

CalciumCell AdhesionCell LineGene Expression RegulationHumansHuman T-lymphotropic virus 1Intercellular Adhesion Molecule-1Lymphocyte Function-Associated Antigen-1Multigene FamilyOncogene Proteins, ViralProtein BindingT-LymphocytesTranscription FactorsViral Regulatory and Accessory ProteinsCalciumIntercellular Adhesion Molecule-1Lymphocyte Function-Associated Antigen-1Oncogene Proteins, Viralp12I protein, Human T-lymphotropic virus 1Transcription FactorsViral Regulatory and Accessory Proteins

Identifiers

PMID16622014
PMCPMC2668115
OpenAlexW1573101036

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.