ArticleJournal of immunology (Baltimore, Md. : 1950)2008
Transmigration of neutrophils across inflamed endothelium is signaled through LFA-1 and Src family kinase.
Article in Journal of immunology (Baltimore, Md. : 1950), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
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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.
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.
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Who cites it
16 citing papers in PubMed, 34 citations in OpenAlex.
- Advanced Nanoparticle Therapeutics for Targeting Neutrophils in Inflammatory Diseases.Advanced healthcare materials · 2025Review
- Article
- STIM1/2 maintain signaling competence at ER-PM contact sites during neutrophil spreading.The Journal of cell biology · 2025Article
- Bletinib ameliorates neutrophilic inflammation and lung injury by inhibiting Src family kinase phosphorylation and activity.British journal of pharmacology · 2021Article
- Peroxiredoxin6 in Endothelial Signaling.Antioxidants (Basel, Switzerland) · 2019Review
- Mechanical features of endothelium regulate cell adhesive molecule-induced calcium response in neutrophils.APL bioengineering · 2019Article
- The Src family kinases Hck, Fgr, and Lyn are critical for the generation of the in vivo inflammatory environment without a direct role in leukocyte recruitment.The Journal of experimental medicine · 2014Article
- Leukocyte function antigen-1, kindlin-3, and calcium flux orchestrate neutrophil recruitment during inflammation.Journal of immunology (Baltimore, Md. : 1950) · 2012Article
- Uropod elongation is a common final step in leukocyte extravasation through inflamed vessels.The Journal of experimental medicine · 2012Article
- Chemokines, selectins and intracellular calcium flux: temporal and spatial cues for leukocyte arrest.Frontiers in immunology · 2012Article
- Leukocyte rolling and adhesion both contribute to regulation of microvascular permeability to albumin via ligation of ICAM-1.American journal of physiology. Cell physiology · 2011Article
- Migrational guidance of neutrophils is mechanotransduced via high-affinity LFA-1 and calcium flux.Journal of immunology (Baltimore, Md. : 1950) · 2011Article
- Src phosphorylation of endothelial cell surface intercellular adhesion molecule-1 mediates neutrophil adhesion and contributes to the mechanism of lung inflammation.Arteriosclerosis, thrombosis, and vascular biology · 2011Article
- ICAM-1 mediates surface contact between neutrophils and keratocytes following corneal epithelial abrasion in the mouse.Experimental eye research · 2010Article
- Breaching multiple barriers: leukocyte motility through venular walls and the interstitium.Nature reviews. Molecular cell biology · 2010Review
- Assessing the barriers to image-guided drug delivery.Wiley interdisciplinary reviews. Nanomedicine and nanobiotechnologyReview
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Leukocyte capture on inflamed endothelium is facilitated by a shift in LFA-1 from low to high affinity that supports binding to ICAM-1. LFA-1 bonds help anchor polymorphonuclear leukocytes (PMN) to inflamed endothelium in shear flow, and their redistribution to the leading edge guides pseudopod formation, migration, and extravasation. These events can be disrupted at the plasma membrane by stabilizing LFA-1 in a low- or intermediate-affinity state with allosteric small molecules. We hypothesized that a minimum dimeric bond formation between high-affinity LFA-1 and ICAM-1 under shear stress is necessary to catalyze transmembrane signaling of directed cell migration. Microspheres and substrates were derivatized with monomeric or dimeric ICAM-1 to simulate the surface of inflamed endothelium under defined ligand valence. Binding to dimeric ICAM-1, and not monomeric ICAM-1, was sufficient to elicit assembly of F-actin and phosphorylation of Src family kinases that colocalized with LFA-1 on adherent PMN. Genetic deletion or small molecule inhibition of Src family kinases disrupted their association with LFA-1 that correlated with diminished polarization of arrested PMN and abrogation of transmigration on inflamed endothelium. We conclude that dimeric bond clusters of LFA-1/ICAM-1 provide a key outside-in signal for orienting cytoskeletal dynamics that direct PMN extravasation at sites of inflammation.
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Registered trials
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.