Evidence map›Paper›PMID 23911404›Full record

ArticleMolecular immunology2013

Neuroimmune semaphorin 4D is necessary for optimal lung allergic inflammation.

K Shanks, E H Nkyimbeng-Takwi, E Smith, M M Lipsky, L J DeTolla, D W Scott, A D Keegan, S P Chapoval

Abstract read
In one paragraph

Article in Molecular immunology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

16 citing papers in PubMed, 33 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Identifying Function Determining Residues in Neuroimmune Semaphorin 4A.International journal of molecular sciences · 2022
    Article
  6. Review
  7. Article
  8. Sja-miR-71a inJournal of extracellular vesicles · 2020
    Article
  9. Article
  10. Neuroimmune semaphorins as costimulatory molecules and beyond.Molecular medicine (Cambridge, Mass.) · 2018
    Review
  11. Review
  12. Article
  13. Semaphorins 4A and 4D in chronic inflammatory diseases.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2017
    Review
  14. Article
  15. Review
  16. Semaphorins and plexins as therapeutic targets.Nature reviews. Drug discovery · 2014
    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

8 authors at 1 institution in 1 country.

K ShanksCenter for Vascular and Inflammatory Diseases, University of Maryland School of Medicine, Baltimore, MD, USA.
E H Nkyimbeng-Takwi
E Smith
M M Lipsky
L J DeTolla
D W Scott
A D Keegan
S P Chapoval
University of Maryland, Baltimore · US

Funding

Immune Semaphorins in Allergic Airway InflammationR21AI076736 · NIAID · UNIVERSITY OF MARYLAND BALTIMORE · PI CHAPOVAL, SVETLANA P. · 2009 to 2010
$413k
NIAID NIH HHS R21 AI076736NIAID NIH HHS R21AI076736
6 · The paper itself

Abstract

Neuroimmune semaphorin 4D (Sema4D) was found to be expressed and function in the nervous and immune systems. In the immune system, Sema4D is constitutively expressed on T cells and regulates T cell priming. In addition, it displays a stimulatory function on macrophages, DC, NK cells, and neutrophils. As all these cells are deeply involved in asthma pathology, we hypothesized that Sema4D plays a critical non-redundant regulatory role in allergic airway response. To test our hypothesis, we exposed Sema4D(-/-) and WT mice to OVA injections and challenges in the well-defined mouse model of OVA-induced experimental asthma. We observed a significant decrease in eosinophilic airway infiltration in allergen-treated Sema4D(-/-) mice relative to WT mice. This reduced allergic inflammatory response was associated with decreased BAL IL-5, IL-13, TGFβ1, IL-6, and IL-17A levels. In addition, T cell proliferation in OVA₃₂₃₋₃₃₉-restimulated Sema4D(-/-) cell cultures was downregulated. We also found increased Treg numbers in spleens of Sema4D(-/-) mice. However, airway hyperreactivity (AHR) to methacholine challenges was not affected by Sema4D deficiency in either acute or chronic experimental disease setting. Surprisingly, lung DC number and activation were not affected by Sema4D deficiency. These data provide a new insight into Sema4D biology and define Sema4D as an important regulator of Th2-driven lung pathophysiology and as a potential target for a combinatory disease immunotherapy.

Indexed as

AnimalsAntigens, CDAsthmaBronchoalveolar Lavage FluidCell ProliferationCells, CulturedCytokinesFlow CytometryHumansHypersensitivityLungLymphocyte ActivationLymphocytesMiceMice, Inbred C57BLMice, KnockoutAntigens, CDCD100 antigenCytokinesOvalbuminSemaphorinsAllergenAsthmaCD72Experimental modelsKnockout micePlexin B1Sema4D/CD100Th2 cytokines

Identifiers

PMID23911404
PMCPMC3783523
OpenAlexW2168917805

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.