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Prepublished online as a Blood First Edition Paper on July 10, 2003; DOI 10.1182/blood-2002-12-3791. This Article Full Text (PDF) Supplemental Videos and Tables All Versions of this Article: 2002-12-3791v1 102/9/3262    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Wolf, K. Articles by Friedl, P. Search for Related Content PubMed PubMed Citation Articles by Wolf, K. Articles by Friedl, P. Social Bookmarking                   What's this? Submitted December 17, 2002 Accepted June 19, 2003 Amoeboid shape change and contact guidance: T lymphocyte crawling through fibrillar collagen is independent of matrix remodeling by MMPs and other proteases Katarina Wolf, Regina Mueller, Stefan Borgmann, Eva-B Broecker, and Peter Friedl* Department of Dermatology, University of Wuerzburg, Wuerzburg, Germany Department of Microbiology, University of Tuebingen, Tuebingen, Germany * Corresponding author; email: peter.fr{at}mail.uni-wuerzburg.de. The passage of leukocytes through basement membranes involves proteolytic degradation of extracellular matrix (ECM) components executed by focalized proteolysis. We have investigated whether the migration of leukocytes through three-dimensional collagenous tissue scaffolds requires similar ECM breakdown. Human T blasts and SupT1 lymphoma cells expressed mRNA of MMP-9, MT1-MMP, MT4-MMP, cathepsin L, uPA and uPAR as well as ADAM-9, -10, -11, -15, -17. Upon long-term migration within three-dimensional collagen matrices, however, no in-situ collagenolysis was obtained by sensitive FITC-collagen fragmentation analysis and confocal fluorescence/backscatter microscopy. Consistent with non-proteolytic migration, T cell crawling and path generation were not impaired by protease inhibitor cocktail targeting MMPs, serine proteases, cysteine proteases, and cathepsins. Dynamic imaging of cell-ECM interactions showed T cell migration as an amoeba-like process driven by adaptive morphology, crawling along collagen fibrils (contact guidance), and squeezing through preexisting matrix gaps by vigorous shape change. The concept of nonproteolytic amoeboid migration was confirmed for multi-component collagen lattices containing hyaluronan and chondroitin sulfate and for other migrating leukocytes, including CD8+ T blasts, monocyte-derived dendritic cells, and U937 monocytic cells. Together, amoeboid shape change and contact guidance provide constitutive protease-independent mechanisms for leukocyte trafficking through interstitial tissues that are insensitive towards pharmacologic protease inhibitors. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: P. Friedl and K. Wolf Plasticity of cell migration: a multiscale tuning model J. Cell Biol., December 1, 2009; (2009) jcb.200909003v1. [Abstract] [Full Text] [PDF] Z. Liu, M. Christensson, A. Forslow, I. De Meester, and K.-G. Sundqvist A CD26-Controlled Cell Surface Cascade for Regulation of T Cell Motility and Chemokine Signals J. Immunol., September 15, 2009; 183(6): 3616 - 3624. [Abstract] [Full Text] [PDF] T. Lammermann, J. Renkawitz, X. Wu, K. Hirsch, C. Brakebusch, and M. Sixt Cdc42-dependent leading edge coordination is essential for interstitial dendritic cell migration Blood, June 4, 2009; 113(23): 5703 - 5710. 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