Evidence map›Paper›PMID 7890297›Full record

ArticleImmunology1995

Serotonin regulation of T-cell subpopulations and of macrophage accessory function.

M R Young, J P Matthews

Registry-linked trialOpen access · greenAbstract read
In one paragraph

Article in Immunology, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT01650311 (Investigating Serotonin Signalling in IBD Patients), which is not on this map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
0.9field-weighted citation impact, top 25% 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.

NCT01650311 recruitingnot on this mapstarted 2012, after this paper: background citation

Investigating Serotonin Signalling in IBD Patients

TypeobservationalSponsorMcMaster UniversityRan2012 to 2026Enrolled60ConditionsInflammatory Bowel Disease
3 · Its place in the literature

Who cites it

25 citing papers in PubMed, 90 citations in OpenAlex.

  1. Imipramine Administration inPharmaceuticals (Basel, Switzerland) · 2023
    Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. The Effects of Serotonin in Immune Cells.Frontiers in cardiovascular medicine · 2017
    Review
  9. Immunohistochemical Evaluation of Role of Serotonin in Pathogenesis of Psoriasis.Journal of clinical and diagnostic research : JCDR · 2016
    Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Immunomodulatory effects mediated by serotonin.Journal of immunology research · 2015
    Review
  16. Review
  17. Article
  18. Article
  19. Novel identified receptors on mast cells.Frontiers in immunology · 2012
    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

2 authors at 1 institution in 1 country.

M R YoungResearch Service, Hines VA Hospital, Hines, Illinois.
J P Matthews
Edward Hines, Jr. VA Hospital · US

Funding

PROTEIN PHOSPHATASES-1 AND-2A RESTRICT TUMOR METASTASISR01CA045080 · NCI · LOYOLA UNIVERSITY CHICAGO · PI YOUNG, M. RITA · 1986 to 2001
$389k
MYELOID DIFFERENTIATION THERAPY TO AUGMENT IMMUNOTHERAPYR01CA048080 · NCI · LOYOLA UNIVERSITY CHICAGO · PI YOUNG, M. RITA · 1990 to 1997
–
NCI NIH HHS CA-45080NCI NIH HHS CA-48080
6 · The paper itself

Abstract

The role of serotonin as an immune modulator was investigated by measuring the functional competence of T cells from control mice versus from mice whose intracellular stores of serotonin had been depleted by pretreatment with p-chlorophenylalanine (PCPA). While the proportions of splenic CD4+ and CD8+ T cells isolated from control and PCPA-treated mice were similar, the level of expression of the alpha-chain interleukin-2 receptor (IL-2R) was reduced on splenic CD4+ cells but not on CD8+ cells. Culture with the T-cell mitogen concanavalin A (Con A) failed to induce expression of the IL-2R on either CD4+ or CD8+ cells of PCPA-treated mice, although IL-2R was induced on control cells. The proliferative response to Con A by these spleen cells from PCPA-treated mice was also reduced compared to that by control spleen cells. Both expression of IL-2R and proliferation in response to Con A by spleen cells from serotonin-depleted mice were increased or completely restored by supplementation of the cultures with serotonin. Studies to identify the mechanisms for the reduction in T-cell activation when serotonin levels were reduced implicated a defect in the capacity of macrophages from PCPA-treated mice to provide accessory help for T-cell activation. Splenic macrophages from control mice were able to restore the blastogenic capability of lymphocytes from PCPA-treated mice, although macrophages from PCPA-treated mice were unable to support normal lymphocyte blastogenesis unless the cultures were supplemented with serotonin. These results show the requirement of autologous serotonin for optimal T-cell activation and suggest the importance of serotonin in macrophage accessory function for T-cell activation.

Indexed as

AnimalsCD4-Positive T-LymphocytesCD8-Positive T-LymphocytesCell DivisionCells, CulturedConcanavalin AFemaleFenclonineLymphocyte ActivationMacrophagesMiceMice, Inbred C57BLReceptors, Interleukin-2SerotoninT-LymphocytesConcanavalin AFenclonineReceptors, Interleukin-2Serotonin

Identifiers

PMID7890297
PMCPMC1415171
OpenAlexW2406894639

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.