Cytoskeletal tension actively sustains the migratory T‐cell synaptic contact
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 unde...
| প্রধান লেখক: | , , , , , , , , , |
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| অন্যান্য লেখক: | |
| বিন্যাস: | প্রবন্ধ |
| ভাষা: | English |
| প্রকাশিত: |
EMBO
2020
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| অনলাইন ব্যবহার করুন: | https://hdl.handle.net/1721.1/126042 |
| _version_ | 1826205840590241792 |
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| author | Kumari, Sudha Mak, Michael Poh, Yeh Chuin Tohme, Mira Watson, Nicki Melo, Mariane Bandeira Janssen, Erin Dustin, Michael Geha, Raif Irvine, Darrell J |
| author2 | Massachusetts Institute of Technology. Department of Mechanical Engineering |
| author_facet | Massachusetts Institute of Technology. Department of Mechanical Engineering Kumari, Sudha Mak, Michael Poh, Yeh Chuin Tohme, Mira Watson, Nicki Melo, Mariane Bandeira Janssen, Erin Dustin, Michael Geha, Raif Irvine, Darrell J |
| author_sort | Kumari, Sudha |
| collection | MIT |
| description | 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. |
| first_indexed | 2024-09-23T13:19:57Z |
| format | Article |
| id | mit-1721.1/126042 |
| institution | Massachusetts Institute of Technology |
| language | English |
| last_indexed | 2024-09-23T13:19:57Z |
| publishDate | 2020 |
| publisher | EMBO |
| record_format | dspace |
| spelling | mit-1721.1/1260422022-09-28T13:27:32Z Cytoskeletal tension actively sustains the migratory T‐cell synaptic contact Kumari, Sudha Mak, Michael Poh, Yeh Chuin Tohme, Mira Watson, Nicki Melo, Mariane Bandeira Janssen, Erin Dustin, Michael Geha, Raif Irvine, Darrell J Massachusetts Institute of Technology. Department of Mechanical Engineering Massachusetts Institute of Technology. Department of Biological Engineering Koch Institute for Integrative Cancer Research at MIT 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. 2020-07-01T19:46:47Z 2020-07-01T19:46:47Z 2020-01 2019-11 2020-03-11T14:28:10Z Article http://purl.org/eprint/type/JournalArticle 0261-4189 1460-2075 https://hdl.handle.net/1721.1/126042 Kumari, Sudha et al. "Cytoskeletal tension actively sustains the migratory T‐cell synaptic contact." EMBO Journal 39, 5 (January 2020): e102783 © 2020 The Authors en http://dx.doi.org/10.15252/embj.2019102783 EMBO Journal Creative Commons Attribution 4.0 International license https://creativecommons.org/licenses/by/4.0/ application/pdf EMBO EMBO Press |
| spellingShingle | Kumari, Sudha Mak, Michael Poh, Yeh Chuin Tohme, Mira Watson, Nicki Melo, Mariane Bandeira Janssen, Erin Dustin, Michael Geha, Raif Irvine, Darrell J Cytoskeletal tension actively sustains the migratory T‐cell synaptic contact |
| title | Cytoskeletal tension actively sustains the migratory T‐cell synaptic contact |
| title_full | Cytoskeletal tension actively sustains the migratory T‐cell synaptic contact |
| title_fullStr | Cytoskeletal tension actively sustains the migratory T‐cell synaptic contact |
| title_full_unstemmed | Cytoskeletal tension actively sustains the migratory T‐cell synaptic contact |
| title_short | Cytoskeletal tension actively sustains the migratory T‐cell synaptic contact |
| title_sort | cytoskeletal tension actively sustains the migratory t cell synaptic contact |
| url | https://hdl.handle.net/1721.1/126042 |
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