Evidence map›Paper›PMID 7507091›Full record

ArticleImmunology1993

Biochemical and functional alterations induced by CD23 ligation in the human promonocytic cell line U937.

N Paul-Eugene, C Amirand, F Ouaaz, J P Ballini, D M Mossalayi, B Dugas, J P Kolb

Open access · greenAbstract read
In one paragraph

Article in Immunology, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.2field-weighted citation impact, top 55% 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

1 citing paper in PubMed, 4 citations in OpenAlex.

  1. 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

7 authors at 1 institution in 1 country.

N Paul-EugeneU196 INSERM, Institut Curie, Paris, France.
C Amirand
F Ouaaz
J P Ballini
D M Mossalayi
B Dugas
J P Kolb
Inserm · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The early events triggered in interleukin-4 (IL-4)-stimulated U937 cells by ligation of CD23/Fc epsilon RII with specific monoclonal antibodies (mAb) were analysed, as a model of the action of this molecule on the differentiation of promonocytic cells. As well as IL-4-activated human monocytes, addition of anti-CD23 mAb to IL-4-treated U937 cells triggered cAMP accumulation but did not evoke significant polyphosphoinositide hydrolysis. However, by a microspectrofluorometric technique allowing single cell analysis, anti-CD23 mAb was found to elicit calcium mobilization in these cells. In addition, the treatment induced phenotypic alterations in these cells, as evidenced by the acquisition of the monocyte marker CD14 and the increase of the alpha-chain (CD11a) and of the common beta-chain (CD18) of the leucocyte function-associated antigen 1 (LFA-1) family antigens. Although weaker than in monocytes, CD23 ligation evoked a small secretion of the pro-inflammatory mediators IL-6 and thromboxane B2. These data suggest that a significant maturation of promonocytic cells towards a more mature monocytic phenotype can be achieved through successive exposure to IL-4 and CD23 ligation.

Indexed as

Antibodies, MonoclonalAntigens, CDAntigens, Differentiation, MyelomonocyticCalciumCD11 AntigensCD18 AntigensCell DivisionCyclic AMPHumansInositol 1,4,5-TrisphosphateInterleukin-4Interleukin-6Leukemia, Monocytic, AcuteLipopolysaccharide ReceptorsMonocytesReceptors, IgEAntibodies, MonoclonalAntigens, CDAntigens, Differentiation, MyelomonocyticCalciumCD11 AntigensCD18 AntigensCyclic AMPInositol 1,4,5-TrisphosphateInterleukin-4Interleukin-6Lipopolysaccharide ReceptorsReceptors, IgEThromboxane B2

Identifiers

PMID7507091
PMCPMC1422235
OpenAlexW2417663983

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.