期刊
JOURNAL OF IMMUNOLOGY
卷 187, 期 7, 页码 3663-3670出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1100103
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资金
- National Institutes of Health/National Institute of Allergy and Infectious Diseases [R01 AI068062]
- Burroughs Wellcome Foundation
- University of Wisconsin Institute on Aging (National Institutes of Health) [T32AG000213-17]
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. The Journal of Immunology, 2011, 187: 3663-3670.
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