Evidence map›Paper›PMID 34335619›Full record

ReviewFrontiers in immunology2021

The Role of T Cell Senescence in Neurological Diseases and Its Regulation by Cellular Metabolism.

Johannes Fessler, Stefano Angiari

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

12 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Review
  6. Article
  7. Review
  8. Review
  9. Review
  10. Immunosenescence of T cells: a key player in rheumatoid arthritis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022
    Review
  11. Review
  12. 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.

Johannes FesslerDivision of Immunology and Pathophysiology, Otto Loewi Research Center, Medical University of Graz, Graz, Austria.
Stefano AngiariDivision of Immunology and Pathophysiology, Otto Loewi Research Center, Medical University of Graz, Graz, Austria.
Medical University of Graz · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Immunosenescence is a state of dysregulated leukocyte function characterised by arrested cell cycle, telomere shortening, expression of markers of cellular stress, and secretion of pro-inflammatory mediators. Immunosenescence principally develops during aging, but it may also be induced in other pathological settings, such as chronic viral infections and autoimmune diseases. Appearance of senescent immune cells has been shown to potentially cause chronic inflammation and tissue damage, suggesting an important role for this process in organismal homeostasis. In particular, the presence of senescent T lymphocytes has been reported in neurological diseases, with some works pointing towards a direct connection between T cell senescence, inflammation and neuronal damage. In this minireview, we provide an overview on the role of T cell senescence in neurological disorders, in particular in multiple sclerosis and Alzheimer disease. We also discuss recent literature investigating how metabolic remodelling controls the development of a senescence phenotype in T cells. Targeting metabolic pathways involved in the induction of senescent T cells may indeed represent a novel approach to limit their inflammatory activity and prevent neuroinflammation and neurodegeneration.

Indexed as

AnimalsHumansImmunosenescenceNerve DegenerationNeuroinflammatory DiseasesT-LymphocytesimmunometabolismimmunosenescenceneurodegenerationneuroinflammationT cell

Identifiers

PMID34335619
PMCPMC8317490
OpenAlexW3179760435

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.