Evidence map›Paper›PMID 9616382›Full record

ArticleImmunology1998

Signalling through NK1.1 triggers NK cells to die but induces NK T cells to produce interleukin-4.

A Asea, J Stein-Streilein

Open access · bronzeAbstract read
In one paragraph

Article in Immunology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

10 citing papers in PubMed, 41 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. CD8+ cells suppress oil-induced arthritis.Clinical and experimental immunology · 2000
    Article
  8. Article
  9. Article
  10. 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

2 authors at 2 institutions in 1 country.

A AseaDepartment of Medicine, University of Miami School of Medicine, FL, USA.
J Stein-Streilein
Pulmonary and Critical Care Associates · USUniversity of Miami · US

Funding

PULMONARY INTERTITIAL DISEASE BY HAPTENSR01HL033709 · NHLBI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI STEIN-STREILEIN, JOAN · 1987 to 1996
–
NHLBI NIH HHS HL33709
6 · The paper itself

Abstract

In vivo inoculation of specific antibody is an accepted protocol for elimination of specific cell populations. Except for anti-CD3 and anti-CD4, it is not known if the depleted cells are eliminated by signalling through the target molecule or through a more non-specific mechanism. C57BL/6 mice were inoculated with anti-natural killer (NK1.1) monoclonal antibody (mAb). Thereafter spleen cells were harvested, stained for both surface and intracellular markers, and analysed by flow cytometry. As early as 2 hr post inoculation, NK cells were signalled to become apoptotic while signalling through the NK1.1 molecule activated NK1.1+ T-cell receptor (TCR)+ (NK T) cells to increase in number, and produce interleukin-4 (IL-4). Anti NK1.1 mAb was less efficient at signalling apoptosis in NK cells when NK T-cell deficient [beta 2-microglobulin beta 2m-deficient] mice were used compared with wild type mice. Efficient apoptotic signalling was restored when beta 2m-deficient mice were reconstituted with NK T cells. NK-specific antibody best signals the apoptotic process in susceptible NK cells when resistant NK T cells are present, activated, and secrete IL-4.

Indexed as

AnimalsAntibodies, MonoclonalAntigensAntigens, LyAntigens, SurfaceApoptosisFemaleInterleukin-4Killer Cells, NaturalLectins, C-TypeMiceMice, Inbred BALB CMice, Inbred C57BLNK Cell Lectin-Like Receptor Subfamily BProteinsSignal TransductionAntibodies, MonoclonalAntigensAntigens, LyAntigens, SurfaceInterleukin-4Klrb1c protein, mouseLectins, C-TypeNK Cell Lectin-Like Receptor Subfamily BProteins

Identifiers

PMID9616382
PMCPMC1364192
OpenAlexW1505335753

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.