Evidence map›Paper›PMID 25950471›Full record

ArticleCell death & disease2015

FAS-ligand regulates differential activation-induced cell death of human T-helper 1 and 17 cells in healthy donors and multiple sclerosis patients.

M T Cencioni, S Santini, G Ruocco, G Borsellino, M De Bardi, M G Grasso, S Ruggieri, C Gasperini, D Centonze, D Barilá and 2 more

Erratum issuedOpen 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. An erratum has been issued. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.0field-weighted citation impact, top 9% 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, 39 citations in OpenAlex.

  1. Article
  2. Article
  3. Cell death in multiple sclerosis.Cell death and differentiation · 2026
    Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Effector T Cells in Multiple Sclerosis.Cold Spring Harbor perspectives in medicine · 2018
    Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors at 2 institutions in 1 country.

M T CencioniNeuroimmunology Unit, Santa Lucia Foundation, Rome, Italy.
S Santini1] Cell Signaling Unit, Santa Lucia Foundation, Rome, Italy [2] Multiple Sclerosis Centre, Santa Lucia Foundation, Rome, Italy.
G RuoccoNeuroimmunology Unit, Santa Lucia Foundation, Rome, Italy.
G BorsellinoNeuroimmunology Unit, Santa Lucia Foundation, Rome, Italy.
M De BardiNeuroimmunology Unit, Santa Lucia Foundation, Rome, Italy.
M G GrassoDepartment of Biology, University Tor Vergata, Rome, Italy.
S RuggieriDepartment of Neuroscience, University Tor Vergata, Rome, Italy.
C GasperiniDepartment of Neuroscience, University Tor Vergata, Rome, Italy.
D Centonze1] Department of Neuroscience "Lancisi", San Camillo Hospital, Rome, Italy [2] Neuroimmunology and Synaptic Plasticity Unit, Santa Lucia Foundation, Rome, Italy.
D Barilá1] Cell Signaling Unit, Santa Lucia Foundation, Rome, Italy [2] Multiple Sclerosis Centre, Santa Lucia Foundation, Rome, Italy.
L BattistiniNeuroimmunology Unit, Santa Lucia Foundation, Rome, Italy.
E VolpeNeuroimmunology Unit, Santa Lucia Foundation, Rome, Italy.
Fondazione Santa Lucia · ITUniversity of Rome Tor Vergata · IT

Funding

Telethon GGP07252
6 · The paper itself

Abstract

Functionally distinct T-helper (Th) subsets orchestrate immune responses. Maintenance of homeostasis through the tight control of inflammatory Th cells is crucial to avoid autoimmune inflammation. Activation-Induced Cell Death (AICD) regulates homeostasis of T cells, and it has never been investigated in human Th cells. We generated stable clones of inflammatory Th subsets involved in autoimmune diseases, such as Th1, Th17 and Th1/17 cells, from healthy donors (HD) and multiple sclerosis (MS) patients and we measured AICD. We find that human Th1 cells are sensitive, whereas Th17 and Th1/17 are resistant, to AICD. In particular, Th1 cells express high level of FAS-ligand (FASL), which interacts with FAS and leads to caspases' cleavage and ultimately to cell death. In contrast, low FASL expression in Th17 and Th1/17 cells blunts caspase 8 activation and thus reduces cell death. Interestingly, Th cells obtained from healthy individuals and MS patients behave similarly, suggesting that this mechanism could explain the persistence of inflammatory IL-17-producing cells in autoimmune diseases, such as MS, where their generation is particularly substantial.

Indexed as

AdultApoptosisCase-Control StudiesCell DeathFas Ligand ProteinFemaleHumansMaleMultiple SclerosisTh17 CellsTh1 CellsTissue DonorsFASLG protein, humanFas Ligand Protein

Identifiers

PMID25950471
PMCPMC4669684
OpenAlexW1520378235

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.