Chemokines are a large family (~ 50 members) of chemoattractants that bind to cognate chemokine receptors (~ 25 known). Leukocytes roll along the vascular endothelium through selectins interacting with their glycoprotein ligands until they encounter a chemokine that stops them in their tracks (1, 2). The fact that chemokines can induce arrest of rolling leukocytes and make them adhere was discovered in the 1990s (3–6), and the term “arrest chemokines” was coined in 2003 (7). Many chemokines including CXCL1, 2, 8, 9, 10, 12, CCL 3, 5, 11, 19, 21, and CX3CL1 have been shown to activate leukocyte integrins and induce arrest, but other chemokines may also have this ability and simply have not been tested in rolling-to-arrest assays. In this Research Topic, 26 authors have contributed 9 articles touching on many of the known arrest chemokines. This Research Topic is aimed at covering the structure, expression, and physiological function of arrest chemokines, the biophysical processes associated with leukocyte arrest, and the molecular mechanisms of rapid leukocyte integrin activation responsible for arrest.

Bongrand’s group has pioneered the study of the biomechanics of cell adhesion for the past 30 years (8). In their contribution to this Research Topic (9), they discuss the finite time required for integrin activation, the nanoscale dynamics of the arrest process, and the contribution of local membrane deformation. They apply this knowledge of the biomechanics of leukocyte arrest to the study of the leukocyte arrest defect seen in patients with leukocyte adhesion deficiency (LAD) type III. In this disorder, the cytoskeletal protein kindlin-3 is not expressed and integrin activation is impaired.