Evidence map›Paper›PMID 26203857›Full record

ArticleCell death & disease2015

Role of acid sphingomyelinase bioactivity in human CD4+ T-cell activation and immune responses.

A Bai, E Kokkotou, Y Zheng, S C Robson

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

21 citing papers in PubMed, 41 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Acid Sphingomyelinase Deficiency: A Clinical and Immunological Perspective.International journal of molecular sciences · 2021
    Review
  6. Ceramides in Skin Health and Disease: An Update.American journal of clinical dermatology · 2021
    Review
  7. Article
  8. Review
  9. Article
  10. Review
  11. Review
  12. Review
  13. Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Inhibition of neddylation ameliorates DSS-induced colitis.Cellular & molecular immunology · 2018
    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 2 institutions in 1 country.

A BaiDivision of Gastroenterology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard University, Boston, MA, USA.
E KokkotouDivision of Gastroenterology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard University, Boston, MA, USA.
Y ZhengDepartment of Surgery, Beth Israel Deaconess Medical Center, Harvard University, Boston, MA, USA.
S C RobsonDivision of Gastroenterology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard University, Boston, MA, USA.
Harvard University · USBeth Israel Deaconess Medical Center · US

Funding

VASCULAR TOPOGRAPHY OF CD39/NTPDASESP01HL076540 · NHLBI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI AIRD, WILLIAM C · 2004 to 2014
$20.3M
Purinergic ThromboregulationR01HL094400 · NHLBI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI ROBSON, SIMON C. · 2009 to 2010
$1.4M
NHLBI NIH HHS P01 HL076540NHLBI NIH HHS P01-HL076540NHLBI NIH HHS R01 HL094400NHLBI NIH HHS R01-HL094400
6 · The paper itself

Abstract

Acid sphingomyelinase (ASM), a lipid hydrolase enzyme, has the potential to modulate various cellular activation responses via the generation of ceramide and by interaction with cellular receptors. We have hypothesized that ASM modulates CD4(+) T-cell receptor activation and impacts immune responses. We first observed interactions of ASM with the intracellular domains of both CD3 and CD28. ASM further mediates T-cell proliferation after anti-CD3/CD28 antibody stimulation and alters CD4(+) T-cell activation signals by generating ceramide. We noted that various pharmacological inhibitors of ASM or knockdown of ASM using small hairpin RNA inhibit CD3/CD28-mediated CD4(+) T-cell proliferation and activation. Furthermore, such blockade of ASM bioactivity by biochemical inhibitors and/or molecular-targeted knockdown of ASM broadly abrogate T-helper cell responses. In conclusion, we detail immune, pivotal roles of ASM in adaptive immune T-cell responses, and propose that these pathways might provide novel targets for the therapy of autoimmune and inflammatory diseases.

Indexed as

Adaptive ImmunityAmitriptylineAntibodiesCarnitineCD28 AntigensCD3 ComplexCell ProliferationCeramidesEnzyme InhibitorsGene Expression RegulationHumansImipramineLymphocyte ActivationPrimary Cell CultureProtein BindingProtein Structure, TertiaryAmitriptylineAntibodiesCarnitineCD28 AntigensCD3 ComplexCeramidesEnzyme InhibitorsImipramineReceptors, Antigen, T-CellRNA, Small InterferingSphingomyelin Phosphodiesterase

Identifiers

PMID26203857
PMCPMC4650726
OpenAlexW1597744339

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.