Evidence map›Paper›PMID 9292968›Full record

ReviewTrends in neurosciences1997

T-cell apoptosis in autoimmune diseases: termination of inflammation in the nervous system and other sites with specialized immune-defense mechanisms.

R Gold, H P Hartung, H Lassmann

Abstract readReview
In one paragraph

Review in Trends in neurosciences, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
–field-weighted citation impact
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

28 citing papers in PubMed.

  1. The neuropathobiology of multiple sclerosis.Nature reviews. Neuroscience · 2024
    Review
  2. Protective Role of a New Polysaccharide Extracted fromBioMed research international · 2021
    Article
  3. Multiple sclerosis.Nature reviews. Disease primers · 2018
    Review
  4. The Neuro-Immune-Regulators (NIREGs) Promote Tissue Resilience; a Vital Component of the Host's Defense Strategy against Neuroinflammation.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2018
    Review
  5. Article
  6. Review
  7. Review
  8. Review
  9. Review
  10. Article
  11. Genetic deficiency of Irgm1 (LRG-47) suppresses induction of experimental autoimmune encephalomyelitis by promoting apoptosis of activated CD4+ T cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2010
    Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. New immunopathologic insights into multiple sclerosis.Current neurology and neuroscience reports · 2003
    Review
  17. Neuronal survival after CNS insult is determined by a genetically encoded autoimmune response.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2001
    Article
  18. Article
  19. 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

3 authors.

R GoldDept of Neurology, Clinical Research Unit for Multiple Sclerosis, Würzburg, Germany.
H P Hartung
H Lassmann

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We have studied T-cell apoptosis in animal models of human autoimmune disorders of the nervous system and in other tissues devoid of specialized immune-defense mechanisms. Our data suggest that the CNS has high potential for elimination of T-cell-dependent inflammation, whereas this mechanism is less effective in the PNS, and is almost absent in other tissues such as muscle and skin. Interestingly, several conventional and novel immunotherapeutic approaches, such as glucocorticosteroid and high-dose antigen therapy, induce T-cell apoptosis in situ. In vitro experiments suggest different scenarios for the mechanisms by which specific cellular and humoral elements in the nervous system synergize and sensitize T cells for apoptosis in vivo. We also discuss regulatory, proapoptotic mechanisms, such as the Fas-FasL system and galectin-I, that have been utilized in other tissues to mediate immune protection.

Indexed as

AnimalsApoptosisAutoimmune DiseasesHumansImmune SystemInflammationNervous SystemNervous System Physiological PhenomenaT-Lymphocytes

Identifiers

PMID9292968
PMCPMC7127798

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.