Arrestin makes T cells stop and become active

Vsevolod V Gurevich1, Eugenia V Gurevich

  • 1Department of Pharmacology, Vanderbilt University, Nashville, TN, USA.

The EMBO Journal
|February 8, 2014
PubMed

T-cell activation requires signaling by T-cell receptors (TCRs) that bind antigen on the antigen-presenting cells (APCs) at the immunological synapse (IS). Sustained signaling requires continuous supply of new TCRs to the IS. In this issue of The EMBO Journal, Fernández-Arenas et al (2014) describe a novel role of β-arrestin-1 at the IS periphery: endocytosis of TCRs and chemokine CXCR4 receptors. Internalized TCRs are then delivered to the IS, where they engage antigen and support prolonged signaling, whereas CXCR4 internalization stops T-cell migration.

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