Evidence map›Paper›PMID 7511685›Full record

ArticleThe Journal of experimental medicine1994

Stimulation of integrin-mediated adhesion of T lymphocytes and monocytes: two mechanisms with divergent biological consequences.

R J Faull, N L Kovach, J M Harlan, M H Ginsberg

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 1994. 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
5.1field-weighted citation impact, top 4% 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, 142 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Invariant chain induces B cell maturation in a process that is independent of its chaperonic activity.Proceedings of the National Academy of Sciences of the United States of America · 2002
    Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  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

4 authors at 1 institution in 1 country.

R J FaullCommittee on Vascular Biology, Scripps Research Institute, La Jolla, California 92037.
N L Kovach
J M Harlan
M H Ginsberg
Scripps Research Institute · US

Funding

REGULATION OF SECOND MESSENGERS BY BETA3 INTEGRINS IN THE VASCULAR SYSTEMP01HL048728 · NHLBI · SCRIPPS RESEARCH INSTITUTE · PI GINSBERG, MARK HOWARD · 1992 to 2003
$7.4M
Regulation of Integrin Alpha4 BetalR01AR027214 · NIAMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI GINSBERG, MARK HOWARD · 1986 to 2010
$3.5M
PLATELETS IN RHEUMATIC DISEASER37AR027214 · NIAMS · SCRIPPS RESEARCH INSTITUTE · PI GINSBERG, MARK HOWARD · 1991 to 2000
$279k
PLASMA FIBRONECTIN IN PLATELET HEMOSTATIC FUNCTIONR01HL028235 · NHLBI · SCRIPPS RESEARCH INSTITUTE · PI GINSBERG, MARK HOWARD · 1985 to 1994
–
NHLBI NIH HHS HL-28235NHLBI NIH HHS HL-48728NIAMS NIH HHS AR-27214
6 · The paper itself

Abstract

We show that the adhesion of T lymphoid cells to immobilized fibronectin can be increased by two distinct mechanisms. The first is by increasing the affinity of the fibronectin receptor/ligand interaction using the anti-beta 1 integrin monoclonal antibody 8A2. The second is by treating the cells with phorbol 12-myristate 13-acetate (PMA), which alters events that occur after receptor occupancy (e.g., cell spreading) without affecting receptor affinity. The effects of these two mechanisms on adhesion in the presence of physiological concentrations of soluble fibronectin suggest that they have different biological consequences. Under these conditions, the net effect of increasing the affinity of the fibronectin receptors is to decrease cell adhesion, whereas the increase in adhesion induced by PMA is unaffected. This suggests that the high affinity receptors are not primarily available for cell adhesion under these circumstances, and that they have an alternative function. We further show that high affinity binding of soluble fibronectin can be induced by either differentiation of the monocytic cell line THP-1 or by cross-linking the T cell receptor complexes on the T lymphoid cell line HUT-78. The differentiated monocytic cells express two populations of fibronectin receptors: a minority in a high affinity state, and the majority in a low affinity state. Thus they will both continue to adhere in the presence of physiological concentrations of soluble fibronectin and bind significant amounts of soluble fibronectin at the cell surface.

Indexed as

AnimalsAntibodies, MonoclonalCell AdhesionCell DifferentiationFibronectinsHumansIntegrin alpha4beta1Integrin beta1IntegrinsMiceMonocytesReceptors, FibronectinSolubilityTetradecanoylphorbol AcetateT-LymphocytesAntibodies, MonoclonalFibronectinsIntegrin alpha4beta1Integrin beta1IntegrinsReceptors, FibronectinTetradecanoylphorbol Acetate

Identifiers

PMID7511685
PMCPMC2191445
OpenAlexW1972287742

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.