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Confinement-optimized three-dimensional T cell amoeboid motility is modulated via myosin IIA-regulated adhesions.

During trafficking through tissues, T cells fine-tune their motility to balance the extent and duration of cell-surface contacts versus the need to traverse an entire organ. Here we show that in vivo, myosin IIA-deficient T cells had a triad of defects, including overadherence to high-endothelial venules, less interstitial migration and inefficient completion of recirculation through lymph nodes. Spatiotemporal analysis of three-dimensional motility in microchannels showed that the degree of confinement and myosin IIA function, rather than integrin adhesion (as proposed by the haptokinetic model), optimized motility rate. This motility occurred via a myosin IIA-dependent rapid 'walking' mode with multiple small and simultaneous adhesions to the substrate, which prevented spurious and prolonged adhesions. Adhesion discrimination provided by myosin IIA is thus necessary for the optimization of motility through complex tissues.

Pubmed ID: 20835229


  • Jacobelli J
  • Friedman RS
  • Conti MA
  • Lennon-Dumenil AM
  • Piel M
  • Sorensen CM
  • Adelstein RS
  • Krummel MF


Nature immunology

Publication Data

October 21, 2010

Associated Grants

  • Agency: NIAID NIH HHS, Id: AI52116
  • Agency: NIAID NIH HHS, Id: R01 AI052116
  • Agency: NIAID NIH HHS, Id: R01 AI052116-07

Mesh Terms

  • Animals
  • Cell Adhesion
  • Cell Movement
  • Female
  • Lymph Nodes
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Nonmuscle Myosin Type IIA
  • T-Lymphocytes