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Cytoskeletal tension actively sustains the migratory T cell synaptic contact

Sudha Kumari, Michael Mak, Yehchuin Poh, Mira Tohme, Nicki Watson, Mariane Melo, Erin Janssen, Michael Dustin, Raif Geha, Darrell J. Irvine
doi: https://doi.org/10.1101/437236
Sudha Kumari
1Koch Institute of Integrative Research, MIT, Cambridge, MA
2Ragon Institute of Harvard, MIT and MGH, Cambridge, MA
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  • For correspondence: kumars04@mit.edu djirvine@mit.edu
Michael Mak
3Department of Mechanical Engineering, MIT, Cambridge, MA
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Yehchuin Poh
1Koch Institute of Integrative Research, MIT, Cambridge, MA
3Department of Mechanical Engineering, MIT, Cambridge, MA
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Mira Tohme
4Division of Immunology, Boston Children’s Hospital, Harvard Medical School, Boston, MA
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Nicki Watson
5Whitehead Institute of Biomedical Research, Cambridge, MA
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Mariane Melo
1Koch Institute of Integrative Research, MIT, Cambridge, MA
2Ragon Institute of Harvard, MIT and MGH, Cambridge, MA
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Erin Janssen
4Division of Immunology, Boston Children’s Hospital, Harvard Medical School, Boston, MA
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Michael Dustin
6Kennedy Institute of Rheumatology, University of Oxford, Oxford, UK
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Raif Geha
4Division of Immunology, Boston Children’s Hospital, Harvard Medical School, Boston, MA
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Darrell J. Irvine
1Koch Institute of Integrative Research, MIT, Cambridge, MA
2Ragon Institute of Harvard, MIT and MGH, Cambridge, MA
7Department of Biological engineering, MIT, Cambridge, MA
8Howard Hughes Medical Institute, Chevy Chase, MD
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  • For correspondence: kumars04@mit.edu djirvine@mit.edu
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Summary

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 rearrangement 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.

  • Symmetry breaking
  • immunological synapse
  • actin cytoskeleton
  • synapse mechanics
  • T cell migration
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The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under a CC-BY-NC-ND 4.0 International license.
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Posted May 04, 2019.
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Cytoskeletal tension actively sustains the migratory T cell synaptic contact
Sudha Kumari, Michael Mak, Yehchuin Poh, Mira Tohme, Nicki Watson, Mariane Melo, Erin Janssen, Michael Dustin, Raif Geha, Darrell J. Irvine
bioRxiv 437236; doi: https://doi.org/10.1101/437236
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Cytoskeletal tension actively sustains the migratory T cell synaptic contact
Sudha Kumari, Michael Mak, Yehchuin Poh, Mira Tohme, Nicki Watson, Mariane Melo, Erin Janssen, Michael Dustin, Raif Geha, Darrell J. Irvine
bioRxiv 437236; doi: https://doi.org/10.1101/437236

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