title: Arrestin makes T cells stop and become active.
abstract: 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.
authors: Department of Pharmacology, Vanderbilt University, Nashville, TN, USA.
authors: Vsevolod V
authors: VV
authors: Gurevich
authors: Eugenia V
authors: EV
authors: Gurevich
mesh_terms: D000818:Animals; D019390:Arrestins / Q000378:metabolism*; D005786:Gene Expression Regulation / Q000276:immunology*; D006801:Humans; D054992:Immunological Synapses / Q000378:metabolism*; D018448:Models, Immunological; D011948:Receptors, Antigen, T-Cell / Q000378:metabolism*; D015398:Signal Transduction / Q000276:immunology*; D000071559:beta-Arrestin 1; D000071557:beta-Arrestins
chemical_list: C000605253:ARRB1 protein, human; D019390:Arrestins; D011948:Receptors, Antigen, T-Cell; D000071559:beta-Arrestin 1; D000071557:beta-Arrestins