AI Article Synopsis
- Cytotoxic T lymphocytes (CTLs) kill virus-infected and cancer cells via T cell receptor (TCR) recognition, but the process of disengaging to enable multiple kills was unclear.
- TCR activation creates specialized membrane regions that produce diacylglycerol (DAG), which helps in shedding activated TCRs into DAG-enriched ectosomes rather than being internalized.
- These ectosomes are taken up by target cells, leading to the termination of TCR signaling and allowing CTLs to detach and continue their killing activity on other targets.
Article 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.
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7614748 | PMC |
| http://dx.doi.org/10.1126/science.abp8933 | DOI Listing |
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