Journal
SCIENCE IMMUNOLOGY
Volume 4, Issue 31, Pages -Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/sciimmunol.aav1987
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Funding
- CellNetworks Cluster of Excellence [ECX81]
- Deutsche Forschungsgemeinschaft [FA378-1/15-1, SFB1129]
- Deutsche Forschungsgemeinschaft (from the HBIGS graduate school)
- HFSP [RGP0021/2016]
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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.
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