Evidence map›Paper›PMID 26554893›Full record

ReviewCurrent opinion in hematology2016

Regulation of tissue infiltration by neutrophils: role of integrin α3β1 and other factors.

Pallavi Subramanian, Ioannis Mitroulis, George Hajishengallis, Triantafyllos Chavakis

Open access · greenAbstract readReview
In one paragraph

Review in Current opinion in hematology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.8field-weighted citation impact, top 10% 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

18 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
  2. Boosting Sensory Nerve-to-Bone Interactions Enhances Hedgehog Mediated Calvarial Bone Repair.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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  8. β2 Integrins-Multi-Functional Leukocyte Receptors in Health and Disease.International journal of molecular sciences · 2020
    Review
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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 3 institutions in 2 countries.

Pallavi SubramanianaDepartment of Clinical Pathobiochemistry, University Clinic Carl Gustav Carus, TU Dresden, Dresden, Germany bDepartment of Microbiology, Penn Dental Medicine, University of Pennsylvania, Philadelphia, USA *Pallavi Subramanian and Ioannis Mitroulis contributed equally to the writing of this article.
Ioannis Mitroulis
George Hajishengallis
Triantafyllos Chavakis
TU Dresden · DEUniversity Hospital Carl Gustav Carus · DEUniversity of Pennsylvania · US

Funding

P. gingivalis as a keystone pathogenR01DE015254 · NIDCR · UNIVERSITY OF PENNSYLVANIA · PI HAJISHENGALLIS, GEORGIOS · 2004 to 2018
$4.6M
Del-1: Molecular and Cellular Targets in PeriodontitisR01DE024716 · NIDCR · UNIVERSITY OF PENNSYLVANIA · PI HAJISHENGALLIS, GEORGIOS · 2015 to 2019
$2.0M
Novel mechanisms and 'complement-ary' therapy in periodontitisR01DE021685 · NIDCR · UNIVERSITY OF PENNSYLVANIA · PI HAJISHENGALLIS, GEORGIOS · 2012 to 2016
$2.0M
NIDCR NIH HHS DE015254NIDCR NIH HHS DE021685NIDCR NIH HHS DE024716NIDCR NIH HHS R01 DE015254NIDCR NIH HHS R01 DE021685NIDCR NIH HHS R01 DE024716
6 · The paper itself

Abstract

purpose of reviewNeutrophils have traditionally been viewed in the context of acute infection and inflammation forming the first line of defense against invading pathogens. Neutrophil trafficking to the site of inflammation requires adhesion and transmigration through blood vessels, which is orchestrated by adhesion molecules, such as β2 and β1-integrins, chemokines, and cytokines. The review focuses on recent advances in understanding the regulators of neutrophil recruitment during inflammation in both acute and chronic settings. RECENT

findingsRecent findings suggest that besides the established pathways of selectin or chemokine-mediated integrin activation, signaling by distinct Toll-like receptors (TLRs) (especially TLR2, TLR4, and TLR5) can activate integrin-dependent neutrophil adhesion. Moreover, the integrin α3β1 has been vitally implicated as a new player in neutrophil recruitment and TLR-mediated responses in septic inflammation. Furthermore, several endogenous inhibitory mechanisms of leukocyte recruitment have been identified, including the secreted molecules Del-1, PTX3, and GDF-15, which block distinct steps of the leukocyte adhesion cascade, as well as novel regulatory signaling pathways, involving the protein kinase AKT1 and IFN-λ2/IL-28A. SUMMARY: The leukocyte adhesion cascade is a tightly regulated process, subjected to both positive and negative regulators. Dysregulation of this process and hence neutrophil recruitment can lead to the development of inflammatory and autoimmune diseases.

Indexed as

Neutrophil InfiltrationAnimalsCell AdhesionChemokinesHomeostasisHumansIntegrin alpha3beta1NeutrophilsProtein BindingSelectinsSignal TransductionTransendothelial and Transepithelial MigrationChemokinesIntegrin alpha3beta1Selectins

Identifiers

PMID26554893
PMCPMC4668230
OpenAlexW2411295454

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.