ArticleJournal of immunology (Baltimore, Md. : 1950)2009
Vav1 is essential for mechanotactic crawling and migration of neutrophils out of the inflamed microvasculature.
Article in Journal of immunology (Baltimore, Md. : 1950), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 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
57 citing papers in PubMed, 128 citations in OpenAlex.
- The Model of Neutrophil Chemotaxis Participated by the Vascular Endothelial Glycocalyx.International journal of general medicine · 2025Review
- Neutrophil diversity and function in health and disease.Signal transduction and targeted therapy · 2024Review
- Vav family exchange factors: Potential regulator in atherosclerosis.Biochemistry and biophysics reports · 2024Review
- NLRP3 is essential for neutrophil polarization and chemotaxis in response to leukotriene B4 gradient.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Dock2 generates characteristic spatiotemporal patterns of Rac activity to regulate neutrophil polarisation, migration and phagocytosis.Frontiers in immunology · 2023Article
- The Rac-GEF Tiam1 controls integrin-dependent neutrophil responses.Frontiers in immunology · 2023Article
- Not all (cells) who wander are lost: Upstream migration as a pervasive mode of amoeboid cell motility.Frontiers in cell and developmental biology · 2023Review
- Mitofusin-2 regulates leukocyte adhesion and β2 integrin activation.Journal of leukocyte biology · 2022Article
- Specific mesoderm subset derived from human pluripotent stem cells ameliorates microvascular pathology in type 2 diabetic mice.Science advances · 2022Article
- Mimicking of Blood Flow Results in a Distinct Functional Phenotype in Human Non-Adherent Classical Monocytes.Biology · 2021Article
- Regulatory mechanisms of neutrophil migration from the circulation to the airspace.Cellular and molecular life sciences : CMLS · 2021Review
- Neutrophils-From Bone Marrow to First-Line Defense of the Innate Immune System.Frontiers in immunology · 2021Review
- Mechanistic consideration of the effect of perioperative volatile anesthetics on phagocytes.Clinical immunology (Orlando, Fla.) · 2021Review
- Astrocyte- and Neuron-Derived CXCL1 Drives Neutrophil Transmigration and Blood-Brain Barrier Permeability in Viral Encephalitis.Cell reports · 2020Article
- LFA-1 signals to promote actin polymerization and upstream migration in T cells.Journal of cell science · 2020Article
- A Bistable Mechanism Mediated by Integrins Controls Mechanotaxis of Leukocytes.Biophysical journal · 2020Article
- VCAM1/VLA4 interaction mediates Ly6Clow monocyte recruitment to the brain in a TNFR signaling dependent manner during fungal infection.PLoS pathogens · 2020Article
- Human Neutrophils Will Crawl Upstream on ICAM-1 If Mac-1 Is Blocked.Biophysical journal · 2019Article
- Review
- Different Faces for Different Places: Heterogeneity of Neutrophil Phenotype and Function.Journal of immunology research · 2019Review
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 4 countries.
Funding
Abstract
Mac-1-dependent crawling is a new step in the leukocyte recruitment cascade that follows LFA-1-dependent adhesion and precedes emigration. Neutrophil adhesion via LFA-1 has been shown to induce cytoskeletal reorganization through Vav1-dependent signaling, and the current study investigates the role of Vav1 in the leukocyte recruitment process in vivo with particular attention to the events immediately downstream of LFA-1-dependent adhesion. Intravital and spinning-disk-confocal microscopy was used to investigate intravascular crawling in relation to endothelial junctions in vivo in wild-type and Vav1(-/-) mice. Adherent wild-type neutrophils almost immediately began crawling perpendicular to blood flow via Mac-1 until they reached an endothelial junction where they often changed direction. This pattern of perpendicular, mechanotactic crawling was recapitulated in vitro when shear was applied. In sharp contrast, the movement of Vav1(-/-) neutrophils was always in the direction of flow and appeared more passive as if the cells were dragged in the direction of flow in vivo and in vitro. More than 80% of Vav1(-/-) neutrophils moved independent of Mac-1 and could be detached with LFA-1 Abs. An inability to release the uropod was frequently noted for Vav1(-/-) neutrophils, leading to greatly elongated tails. The Vav1(-/-) neutrophils failed to stop or follow junctions and ultimately detached, leading to fewer emigrated neutrophils. The Vav1(-/-) phenotype resulted in fewer neutrophils recruited in a relevant model of infectious peritonitis. Clearly, Vav1 is critical for the complex interplay between LFA-1 and Mac-1 that underlies the programmed intravascular crawling of neutrophils.
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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.