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• W1818990716 startingPage "5509" @default.
• W1818990716 abstract "The adaptive immune response requires interaction between T cells and APC to form a specialized structure termed the immune synapse (IS). Although the TCR is essential for IS organization, other factors such as chemokines participate in this process. In this study, we show that the chemokine CXCL12-mediated signaling contributes to correct IS organization and therefore influences T cell activation. CXCR4 downregulation or blockade on T cells caused defective actin polymerization at the contact site with APC, altered microtubule-organizing center polarization and the IS structure, and reduced T cell/APC contact duration. T cell activation was thus inhibited, as shown by reduced expression of CD25 and CD69 markers and of IL-2 mRNA levels. The results indicate that, through Gi and JAK1 and 2 kinases activation, CXCL12 signaling cooperates to build the IS and to maintain adhesive contacts between APC and T cells, required for continuous TCR signaling." @default.
• W1818990716 created "2016-06-24" @default.
• W1818990716 creator A5009746498 @default.
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• W1818990716 date "2015-06-01" @default.
• W1818990716 modified "2023-10-18" @default.
• W1818990716 title "CXCL12 Regulates through JAK1 and JAK2 Formation of Productive Immunological Synapses" @default.
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• W1818990716 doi "https://doi.org/10.4049/jimmunol.1402419" @default.
• W1818990716 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/25917087" @default.
• W1818990716 hasPublicationYear "2015" @default.
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