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• W2006073149 abstract "The mechanism by which sphingosine-1-phosphate receptor-1 (S1P1) acts to promote lymphocyte egress from lymphoid organs is not defined. Here, we showed that CCR7-deficient T cells left lymph nodes more rapidly than wild-type cells did, whereas CCR7-overexpressing cells were retained for longer. After treatment with FTY720, an agonist that causes downmodulation of lymphocyte S1P1, CCR7-deficient T cells were less effectively retained than wild-type T cells. Moreover, treatment with pertussis toxin to inactivate signaling via G alpha i-protein-coupled receptors restored egress competence to S1P1-deficient lymphocytes. We also found that T cell accumulation in lymph node cortical sinusoids required intrinsic S1P1 expression and was antagonized by CCR7. These findings suggest a model where S1P1 acts in the lymphocyte to promote lymph node egress by overcoming retention signals mediated by CCR7 and additional G alpha i-coupled receptors. Furthermore, by simultaneously upregulating S1P1 and downregulating CCR7, T cells that have divided multiple times switch to a state favoring egress over retention." @default.
• W2006073149 created "2016-06-24" @default.
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• W2006073149 date "2008-01-01" @default.
• W2006073149 modified "2023-10-18" @default.
• W2006073149 title "S1P1 Receptor Signaling Overrides Retention Mediated by Gαi-Coupled Receptors to Promote T Cell Egress" @default.
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• W2006073149 doi "https://doi.org/10.1016/j.immuni.2007.11.017" @default.
• W2006073149 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2691390" @default.
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