ArticleProceedings of the National Academy of Sciences of the United States of America2026
Immune cells employ intermittent integrin-mediated traction forces for 3D migration.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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Who cites it
5 citing papers in PubMed.
- Neutrophils exhibit distinct migration phenotypes that are modulated by transendothelial migration.Communications biology · 2026Article
- Quantifying cell traction forces at the single-fiber scale in 3D: An approach based on deformable photopolymerized fiber arrays.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Mechanobiological engineering strategies for organoid culture.APL bioengineering · 2025Review
- T cells use focal adhesions to pull themselves through confined environments.The Journal of cell biology · 2024Article
- T cells Use Focal Adhesions to Pull Themselves Through Confined Environments.bioRxiv : the preprint server for biology · 2023Article
Corrections and comments
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Authors and funding
19 authors.
Funding
Abstract
To reach targets outside the bloodstream, immune cells can extravasate and migrate through connective tissue. During tissue infiltration, immune cells migrate in an amoeboid fashion, characterized by weak matrix adhesions and low traction forces, that allows them to achieve high migration speeds of up to 10 µm/min. How immune cells reconcile amoeboid migration with the need to overcome steric hindrance in dense matrices is currently not understood. Here we show that NK92 (natural killer) cells can switch from their default amoeboid migration mode to a contractile, mesenchymal-like migration mode when moving through fibrous human amniotic membrane (HAM) tissue. We subsequently study immune cell migration in reconstituted 3D collagen networks with known mechanical properties and pore sizes and apply time-lapse confocal reflection microscopy to obtain simultaneous measurements of migration speed, directional persistence, and cell contractility. We find that NK92 cells exert substantial acto-myosin driven, integrin-mediated contractile forces of up to 100 nN on the extracellular matrix during short contractile phases. This burst-like contractile behavior is also found in primary B, T, NK cells, neutrophils, and monocytes, and is tightly related to the fraction of cells that become stuck in narrow pores of the surrounding matrix. Our results demonstrate that steric hindrance guides the rapid regulation of integrin-mediated adhesion to the ECM in a large number of immune cell subtypes.
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