Evidence map›Paper›PMID 30134791›Full record

ReviewMolecular medicine (Cambridge, Mass.)2018

Neuroimmune semaphorins as costimulatory molecules and beyond.

Svetlana P Chapoval

Open access · goldAbstract readReview
In one paragraph

Review in Molecular medicine (Cambridge, Mass.), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.5field-weighted citation impact, top 41% 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

9 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Astrocyte-to-microglia communication via Sema4B-Plexin-B2 modulates injury-induced reactivity of microglia.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Identifying Function Determining Residues in Neuroimmune Semaphorin 4A.International journal of molecular sciences · 2022
    Article
  8. Review
  9. 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

1 author at 1 institution in 1 country.

Svetlana P ChapovalDepartment of Microbiology and Immunology, University of Maryland School of Medicine, Baltimore, MD, USA. schapoval@som.umaryland.edu.ORCID 0000-0002-7590-4421
University of Mary · US

Funding

Role of Semaphorin 4A in Allergic InflammationR56AI122631 · NIAID · UNIVERSITY OF MARYLAND BALTIMORE · PI KEEGAN, ACHSAH D. · 2016 to 2016
$385k
NIAID NIH HHS R56 AI122631
6 · The paper itself

Abstract

Several neuronal guidance proteins, known as semaphorin molecules, function in the immune system. This dual tissue performance has led to them being defined as "neuroimmune semaphorins". They have been shown to regulate T cell activation by serving as costimulatory molecules. Similar to classical costimulatory molecules, neuroimmune semaphorins are either constitutively or inducibly expressed on immune cells. In contrast to the classical costimulatory molecule function, the action of neuroimmune semaphorins requires the presence of two signals, the first one provided by TCR/MHC engagement, and the second one provided by B7/CD28 interaction. Thus, neuroimmune semaphorins serve as a "signal three" for immune cell activation and regulate the overall intensity of immune response. The current knowledge on their structures, multiple receptors, specific cell/tissue/organ expression, and distinct functions in different diseases are summarized and discussed in this review.

Indexed as

AnimalsHumansNervous SystemSemaphorinsSemaphorinsCostimulationImmune responseInflammationMolecular targetsSemaphorins

Identifiers

PMID30134791
PMCPMC6016892
OpenAlexW2806807230

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.