Evidence map›Paper›PMID 16236124›Full record

ArticleImmunology2005

Costimulation of T-cell proliferation by anti-L-selectin antibody is associated with the reduction of a cdk inhibitor p27.

Ken-Ichi Nishijima, Munetoshi Ando, Shusuke Sano, Aiko Hayashi-Ozawa, Yoshinori Kinoshita, Shinji Iijima

Open access · hybridAbstract read
In one paragraph

Article in Immunology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.8field-weighted citation impact, top 32% 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

7 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. 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

6 authors at 1 institution in 1 country.

Ken-Ichi NishijimaDepartment of Biotechnology, Nagoya University, Nagoya, Japan. nishijma@proc.nubio.nagoya-u.ac.jp
Munetoshi Ando
Shusuke Sano
Aiko Hayashi-Ozawa
Yoshinori Kinoshita
Shinji Iijima
Nagoya University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In this study, we investigated the costimulatory activity of l-selectin in primary mouse T cells. Proliferation induced by immobilized anti-CD3 antibody was enhanced by immobilized anti-l-selectin antibody. In contrast to the anti-CD28 antibody, anti-l-selectin antibody did not enhance interleukin-2 (IL-2) expression. One of the cyclin-dependent kinase (cdk) inhibitors, p27, was reduced by costimulation with anti-l-selectin antibody, as with anti-CD28 antibody, suggesting that the enhancement of T-cell proliferation is the result of a reduced p27 level. Since anti-l-selectin antibody enhanced the activation of extracellular signal-regulated protein kinase (ERK) induced by anti-CD3 antibody, ERK plays an important role in signal integration during costimulation. These results suggest that the mechanism of T-cell costimulation is at least partially different between CD28 and l-selectin, although the two mechanisms share a common downstream event, a reduction of p27 level, as a critical biochemical event in the cell cycle progression of T cells.

Indexed as

AnimalsAntibodies, MonoclonalCell ProliferationCyclin-Dependent Kinase Inhibitor p27Extracellular Signal-Regulated MAP KinasesInterleukin-2L-SelectinLymph NodesLymphocyte ActivationMaleMiceMice, Inbred BALB CReverse Transcriptase Polymerase Chain ReactionSuperantigensT-LymphocytesAntibodies, MonoclonalCyclin-Dependent Kinase Inhibitor p27Extracellular Signal-Regulated MAP KinasesInterleukin-2L-SelectinSuperantigens

Identifiers

PMID16236124
PMCPMC1802426
OpenAlexW2052363629

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.