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• W2151090378 abstract "The T cell migration stop signal is a central step in T cell activation and inflammation; however, its regulatory mechanisms remain largely unknown. Using a live-cell, imaging-based, high-throughput screen, we identified the PG, PGE(2), as a T cell stop signal antagonist. Src kinase inhibitors, microtubule inhibitors, and PGE(2) prevented the T cell stop signal, and impaired T cell-APC conjugation and T cell proliferation induced by primary human allogeneic dendritic cells. However, Src inhibition, but not PGE(2) or microtubule inhibition, impaired TCR-induced ZAP-70 signaling, demonstrating that T cell stop signal antagonists can function either upstream or downstream of proximal TCR signaling. Moreover, we found that PGE(2) abrogated TCR-induced activation of the small GTPase Rap1, suggesting that PGE(2) may modulate T cell adhesion and stopping through Rap1. These results identify a novel role for PGs in preventing T cell stop signals and limiting T cell activation induced by dendritic cells." @default.
• W2151090378 created "2016-06-24" @default.
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• W2151090378 date "2011-09-07" @default.
• W2151090378 modified "2023-10-12" @default.
• W2151090378 title "A Live Imaging Cell Motility Screen Identifies Prostaglandin E₂ as a T Cell Stop Signal Antagonist" @default.
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• W2151090378 doi "https://doi.org/10.4049/jimmunol.1100103" @default.
• W2151090378 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3178752" @default.
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