Evidence map›Paper›PMID 18234059›Full record

ArticleClinical and experimental immunology2008

Leptin promotes cell survival and activates Jurkat T lymphocytes by stimulation of mitogen-activated protein kinase.

P Fernández-Riejos, R Goberna, V Sánchez-Margalet

Open access · greenAbstract read
In one paragraph

Article in Clinical and experimental immunology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
1.5field-weighted citation impact, top 22% 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

31 citing papers in PubMed, 55 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Review
  6. Obesity and the risk of Multiple Sclerosis. The role of Leptin.Annals of clinical and translational neurology · 2021
    Article
  7. Article
  8. Leptin Downregulates Angulin-1 in Active Crohn's Disease via STAT3.International journal of molecular sciences · 2020
    Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Uncovering the liver's role in immunity through RNA co-expression networks.Mammalian genome : official journal of the International Mammalian Genome Society · 2016
    Article
  16. Article
  17. Article
  18. Review
  19. Review
  20. Review
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

3 authors at 2 institutions in 1 country.

P Fernández-RiejosDepartment of Clinical Biochemistry, Virgen Macarena University Hospital, Medical School University of Seville, Seville, Spain.
R Goberna
V Sánchez-Margalet
Hospital Universitario Virgen Macarena · ESUniversidad de Sevilla · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Leptin (Ob) is a non-glycosylated peptide hormone that regulates energy homeostasis centrally, but also has systemic effects including the regulation of the immune function. We have reported previously that leptin activates human peripheral blood lymphocytes co-stimulated with phytohaemagglutinin (PHA) (4 microg/ml), which prevented the employment of pharmacological inhibitors of signalling pathways. In the present study, we used Jurkat T cells that responded to leptin with minimal PHA co-stimulation (0.25 microg/ml). The long isoform of leptin receptor is expressed on Jurkat T cells and upon leptin stimulation, the expression of early activation marker CD69 increases in a dose-dependent manner (0.1-10 nM). We have also found that leptin activates receptor-associated kinases of the Janus family-signal transucers and activators of transcription (JAK-STAT), mitogen-activated protein kinase (MAPK) and phosphatidylinositol 3 kinase (PI3K) signalling pathways. Moreover, we sought to study the possible effect of leptin on cell survival and apoptosis of Jurkat T cells by culture in serum-free conditions. We have assayed the early phases of apoptosis by flow cytometric detection of fluorescein isothiocyanate (FITC)-labelled annexin V simultaneously with dye exclusion of propidium iodide (PI). As well, we have assayed the activation level of caspase-3 by inmunoblot with a specific antibody that recognizes active caspase-3. We have found that leptin inhibits the apoptotic process dose-dependently. By using pharmacological inhibitors, we have found that the stimulatory and anti-apoptotic effects of leptin in Jurkat T cells are dependent on MAPK activation, rather than the PI3K pathway, providing new data regarding the mechanism of action of leptin in T cells, which may be useful to understand more clearly the association between nutritional status and the immune function.

Indexed as

Cell SurvivalDose-Response Relationship, ImmunologicEnzyme ActivationHumansJurkat CellsLeptinLymphocyte ActivationMAP Kinase Signaling SystemMitogen-Activated Protein KinasesNeoplasm ProteinsPhosphatidylinositol 3-KinasesPhosphorylationReceptors, LeptinRecombinant ProteinsReverse Transcriptase Polymerase Chain ReactionSTAT3 Transcription FactorLeptinMitogen-Activated Protein KinasesNeoplasm ProteinsPhosphatidylinositol 3-KinasesReceptors, LeptinRecombinant ProteinsSTAT3 protein, humanSTAT3 Transcription FactorTyrosine

Identifiers

PMID18234059
PMCPMC2276975
OpenAlexW1504068356

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.