English
 
Help Privacy Policy Disclaimer
  Advanced SearchBrowse
  1. View item / 
  2. Item Summary

Item

ITEM ACTIONSEXPORT
Add to Basket
  Local TagsRelease HistoryDetailsSummary

Released
Journal Article

Ectocytosis renders T cell receptor signaling self-limiting at the immune synapse.

MPS-Authors
/persons/resource/persons219478

Nadler,  André
Max Planck Institute for Molecular Cell Biology and Genetics, Max Planck Society;

External Resource
No external resources are shared
Fulltext (restricted access)
There are currently no full texts shared for your IP range.
Fulltext (public)
There are no public fulltexts stored in PuRe
Supplementary Material (public)
There is no public supplementary material available
Citation

Stinchcombe, J. C., Asano, Y., Kaufman, C. J. G., Böhlig, K., Peddie, C. J., Collinson, L. M., et al. (2023). Ectocytosis renders T cell receptor signaling self-limiting at the immune synapse. Science (New York, N.Y.), 380(6647), 818-823. doi:10.1126/science.abp8933.


Cite as: https://hdl.handle.net/21.11116/0000-000E-AADA-D
Abstract
Cytotoxic T lymphocytes (CTLs) kill virus-infected and cancer cells through T cell receptor (TCR) recognition. How CTLs terminate signaling and disengage to allow serial killing has remained a mystery. TCR activation triggers membrane specialization within the immune synapse, including the production of diacylglycerol (DAG), a lipid that can induce negative membrane curvature. We found that activated TCRs were shed into DAG-enriched ectosomes at the immune synapse rather than internalized through endocytosis, suggesting that DAG may contribute to the outward budding required for ectocytosis. Budding ectosomes were endocytosed directly by target cells, thereby terminating TCR signaling and simultaneously disengaging the CTL from the target cell to allow serial killing. Thus, ectocytosis renders TCR signaling self-limiting.