Evidence map›Paper›PMID 35034753›Full record

ReviewHandbook of clinical neurology2022

T cells, α-synuclein and Parkinson disease.

Francesca Garretti, Connor Monahan, Alessandro Sette, Dritan Agalliu, David Sulzer

Open access · greenAbstract readReview
In one paragraph

Review in Handbook of clinical neurology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
59.6field-weighted citation impact, top 1% 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

15 citing papers in PubMed, 49 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
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

5 authors at 2 institutions in 1 country.

Francesca GarrettiDepartment of Pathology, Columbia University Irving Medical Center, New York, NY, United States.
Connor MonahanDepartment of Psychiatry, Columbia University Irving Medical Center, New York, NY, United States.
Alessandro SetteCenter for Autoimmunity and Inflammation, La Jolla Institute for Immunology, La Jolla, CA, United States.
Dritan AgalliuDepartment of Pathology, Columbia University Irving Medical Center, New York, NY, United States; Department of Neurology, Columbia University Irving Medical Center, New York, NY, United States.
David SulzerDepartment of Pathology, Columbia University Irving Medical Center, New York, NY, United States; Department of Psychiatry, Columbia University Irving Medical Center, New York, NY, United States; Department of Pharmacology, Columbia University Irving Medical Center, New York, NY, United States; Division of Molecular Therapeutics, New York State Psychiatric Institute, New York, NY, United States. Electronic address: ds43@cumc.columbia.edu.
Columbia University Irving Medical Center · USLa Jolla Institute for Immunology · US

Funding

Autoimmune Features of Neurodegenerative DisordersR01NS095435 · NINDS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI SETTE, ALESSANDRO, SULZER, DAVID · 2018 to 2022
$4.2M
NINDS NIH HHS R01 NS095435
6 · The paper itself

Abstract

The notion that autoimmune responses to α-synuclein may be involved in the pathogenesis of this disorder stems from reports that mutations in α-synuclein or certain alleles of the major histocompatibility complex (MHC) are associated with the disease and that dopaminergic and norepinephrinergic neurons in the midbrain can present antigenic epitopes. Here, we discuss recent evidence that a defined set of peptides derived from α-synuclein act as antigenic epitopes displayed by specific MHC alleles and drive helper and cytotoxic T cell responses in patients with PD. Moreover, phosphorylated α-synuclein may activate T cell responses in a less restricted manner in PD. While the roles for the acquired immune system in disease pathogenesis remain unknown, preclinical animal models and in vitro studies indicate that T cells may interact with neurons and exert effects related to neuronal death and neuroprotection. These findings suggest that therapeutics that target T cells and ameliorate the incidence or disease severity of inflammatory bowel disorders or CNS autoimmune diseases such as multiple sclerosis may be useful in PD.

Indexed as

alpha-SynucleinParkinson DiseaseAnimalsDopamineHumansNeuronsT-Lymphocytesalpha-SynucleinDopamineCytotoxicDopamineMajor histocompatibility complexMicrogliaRegulatoryT cell

Identifiers

PMID35034753
PMCPMC10193709
OpenAlexW4206095521

What OpenQuestion holds

Textmetadata
LicenceTDM
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.