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| Status |
Public on Nov 15, 2018 |
| Title |
T cell receptor-triggered nuclear actin network formation drives CD4 T cell effector functions |
| Organism |
Homo sapiens |
| Experiment type |
Expression profiling by array
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| Summary |
T cell antigen receptor (TCR) signaling triggers selective cytokine expression to drive T cell proliferation and differentiation required for immune defense and surveillance. The nuclear signaling events responsible for specificity in cytokine gene expression upon T cell activation are largely unknown. Here, we uncover formation of a dynamic actin filament network in the nucleus that regulates cytokine expression for effector functions of CD4 T lymphocytes. TCR engagement triggers the rapid and transient formation of a nuclear actin filament network via nuclear Arp2/3 complex, induced by elevated nuclear Ca2+ levels and regulated via N-Wasp and NIK. Specific interference with TCR-induced formation of nuclear actin filaments impairs production of effector cytokines and prevents generation of antigen-specific antibodies, but does not interfere with immune synapse formation and cell proliferation. Ca2+-regulated actin polymerization in the nucleus allows CD4 T cells the rapid conversion of TCR signals into effector functions required for T cell help
Identification of nuclear F-actin sensitive genes upon TCR signaling
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| Overall design |
4 Donors control (DMSO) treatment (CK-869)
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| Contributor(s) |
Tsopoulidis N, Fackler O |
| Citation(s) |
30610013 |
| Submission date |
Nov 14, 2018 |
| Last update date |
Feb 14, 2019 |
| Contact name |
Nikolaos Tsopoulidis |
| Organization name |
Universitätsklinikum Heidelberg
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| Street address |
Im Neuenheimer Feld 344
|
| City |
Heidelberg |
| ZIP/Postal code |
69120 |
| Country |
Germany |
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| Platforms (1) |
| GPL10558 |
Illumina HumanHT-12 V4.0 expression beadchip |
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| Samples (16)
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| Relations |
| BioProject |
PRJNA505494 |
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