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. 2018 Nov 27;9:2737. doi: 10.3389/fimmu.2018.02737

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Copyright © 2018 Brunner-Weinzierl and Rudd.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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CTLA-4 regulates T-cell motility. (A) Reverse-stop signal model of CTLA-4 (and PD-1). CTLA-4 induces T-cell motility and limits T-cell binding to DCs during antigen-presentation (1, 2). Agonistic CTLA-4 ligation could directly activate the motility of T-cells and thereby interfere with the dwell times of cells with DCs presenting antigenic peptide. PD-1 can function in a similar way (5). (B) CTLA-4 modulates response to chemokines. Chemokine gradients attract T-cells to the site of injury and inflammation. CTLA-4 can alter motility by up-regulating key chemokine receptors CCR5 and CCR7 and the sensitivity toward the chemokines CCL4 (MIP-1β), CXCL12 (SDF1α) and CCL19, but not CXCL9 (MIG) (3). The scheme was drawn using pictures from Servier Medical Art.