Cytoskeletal tension actively sustains the migratory T‐cell synaptic contact
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Kumari_et_al-2020-The_EMBO_Journal.pdf
Description
Published version
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6.35 MB
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Author(s) • • • • • • • • •
Kumari, Sudha
Mak, Michael
Poh, Yeh Chuin
Tohme, Mira
Watson, Nicki
Melo, Mariane Bandeira
Janssen, Erin
Dustin, Michael
Geha, Raif
Irvine, Darrell J
Date Issued
January 2020
Journal
EMBO Journal
Publisher
EMBO
Citation
Kumari, Sudha et al. "Cytoskeletal tension actively sustains the migratory T‐cell synaptic contact." EMBO Journal 39, 5 (January 2020): e102783 © 2020 The Authors
Version
Final published version
Abstract
When migratory T cells encounter antigen-presenting cells (APCs), they arrest and form radially symmetric, stable intercellular junctions termed immunological synapses which facilitate exchange of crucial biochemical information and are critical for T-cell immunity. While the cellular processes underlying synapse formation have been well characterized, those that maintain the symmetry, and thereby the stability of the synapse, remain unknown. Here we identify an antigen-triggered mechanism that actively promotes T-cell synapse symmetry by generating cytoskeletal tension in the plane of the synapse through focal nucleation of actin via Wiskott–Aldrich syndrome protein (WASP), and contraction of the resultant actin filaments by myosin II. Following T-cell activation, WASP is degraded, leading to cytoskeletal unraveling and tension decay, which result in synapse breaking. Thus, our study identifies and characterizes a mechanical program within otherwise highly motile T cells that sustains the symmetry and stability of the T cell–APC synaptic contact.
MIT Department
Massachusetts Institute of Technology. Department of Mechanical Engineering
Massachusetts Institute of Technology. Department of Biological Engineering
Koch Institute for Integrative Cancer Research at MIT
Terms of Use
Creative Commons Attribution 4.0 International license
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DOI of Published Version
https://doi.org/10.15252/embj.2019102783