ArticleBiophysical journal2022
Mechanisms of frustrated phagocytic spreading of human neutrophils on antibody-coated surfaces.
Article in Biophysical journal, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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Who cites it
10 citing papers in PubMed, 14 citations in OpenAlex.
- MERTK coordinates efferocytosis by regulating integrin localization and activation.Journal of cell science · 2026Article
- Antigen-Specific Inverse Vaccination Strategies Using Particle Systems for Multiple Sclerosis.ACS biomaterials science & engineering · 2026Review
- Podosomes and Mechanical Force.Results and problems in cell differentiation · 2026Review
- Neutrophil Heterogeneity in Airway Inflammatory Diseases.Inflammation · 2025Review
- Measurement of macrophage phagocytic capacity by quantifying maximum membrane extension using an opsonized capillary tube assay.Scientific reports · 2025Article
- Potent broadly neutralizing antibodies mediate efficient antibody-dependent phagocytosis of HIV-infected cells.PLoS pathogens · 2024Article
- Particle-based simulations shed light on cytoskeleton-membrane dynamics in phagocytosis.Biophysical journal · 2024Article
- Two-component macrophage model for active phagocytosis with pseudopod formation.Biophysical journal · 2024Article
- Lacking ARHGAP25 mitigates the symptoms of autoantibody-induced arthritis in mice.Frontiers in immunology · 2023Article
- Integrative experimental/computational approach establishes active cellular protrusion as the primary driving force of phagocytic spreading by immune cells.PLoS computational biology · 2022Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Complex motions of immune cells are an integral part of diapedesis, chemotaxis, phagocytosis, and other vital processes. To better understand how immune cells execute such motions, we present a detailed analysis of phagocytic spreading of human neutrophils on flat surfaces functionalized with different densities of immunoglobulin G (IgG) antibodies. We visualize the cell-substrate contact region at high resolution and without labels using reflection interference contrast microscopy and quantify how the area, shape, and position of the contact region evolves over time. We find that the likelihood of the cell commitment to spreading strongly depends on the surface density of IgG, but the rate at which the substrate-contact area of spreading cells increases does not. Validated by a theoretical companion study, our results resolve controversial notions about the mechanisms controlling cell spreading, establishing that active forces generated by the cytoskeleton rather than cell-substrate adhesion primarily drive cellular protrusion. Adhesion, on the other hand, aids phagocytic spreading by regulating the cell commitment to spreading, the maximum cell-substrate contact area, and the directional movement of the contact region.
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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.