Evidence map›Paper›PMID 36874213›Full record

ReviewFrontiers in cellular neuroscience2023

The interplay between T helper cells and brain barriers in the pathogenesis of multiple sclerosis.

Gabriele Angelini, Alessandro Bani, Gabriela Constantin, Barbara Rossi

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in cellular neuroscience, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
9.2field-weighted citation impact, top 2% 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

33 citing papers in PubMed, 36 citations in OpenAlex.

  1. Review
  2. Immune reconstitution and tolerance-inducing therapies as promising therapeutic approaches in multiple sclerosis.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2026
    Review
  3. Article
  4. Review
  5. Review
  6. Natural Killer Cells: Dual Regulators and Therapeutic Targets in Multiple Sclerosis Immunopathogenesis.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2026
    Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Review
  12. Review
  13. Sez6L2 autoimmunity induces cerebellar ataxia in mice.Journal of neuroinflammation · 2025
    Article
  14. Review
  15. Article
  16. Review
  17. Real-world effectiveness and safety of ofatumumab in relapsing-remitting multiple sclerosis: Insights from naïve and switch patients.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025
    Article
  18. Article
  19. Article
  20. 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

4 authors at 1 institution in 1 country.

Gabriele AngeliniDepartment of Medicine, Section of General Pathology, University of Verona, Verona, Italy.
Alessandro BaniDepartment of Medicine, Section of General Pathology, University of Verona, Verona, Italy.
Gabriela ConstantinDepartment of Medicine, Section of General Pathology, University of Verona, Verona, Italy.
Barbara RossiDepartment of Medicine, Section of General Pathology, University of Verona, Verona, Italy.
University of Verona · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The blood-brain barrier (BBB) and the blood-cerebrospinal fluid barrier (BCSFB) represent two complex structures protecting the central nervous system (CNS) against potentially harmful agents and circulating immune cells. The immunosurveillance of the CNS is governed by immune cells that constantly patrol the BCSFB, whereas during neuroinflammatory disorders, both BBB and BCSFB undergo morphological and functional alterations, promoting leukocyte intravascular adhesion and transmigration from the blood circulation into the CNS. Multiple sclerosis (MS) is the prototype of neuroinflammatory disorders in which peripheral T helper (Th) lymphocytes, particularly Th1 and Th17 cells, infiltrate the CNS and contribute to demyelination and neurodegeneration. Th1 and Th17 cells are considered key players in the pathogenesis of MS and its animal model, experimental autoimmune encephalomyelitis. They can actively interact with CNS borders by complex adhesion mechanisms and secretion of a variety of molecules contributing to barrier dysfunction. In this review, we describe the molecular basis involved in the interactions between Th cells and CNS barriers and discuss the emerging roles of dura mater and arachnoid layer as neuroimmune interfaces contributing to the development of CNS inflammatory diseases.

Indexed as

adhesion moleculesblood–brain barrierchoroid plexusmeningeal inflammationmultiple sclerosisneuroinflammationT helper cells

Identifiers

PMID36874213
PMCPMC9975172
OpenAlexW4320921685

What Socratic 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 Socratic graph.