02781nam 2200565 450 991013753110332120230621135640.0(CKB)3710000000569674(oapen)https://directory.doabooks.org/handle/20.500.12854/41301(EXLCZ)99371000000056967420160125h20152015 fy| 0engurmu#---uuuuutxtrdacontentcrdamediacrrdacarrierArrest chemokines[electronic resource] /topic editor: Klaus LeyFrontiers Media SA2015[Lausanne, Switzerland] :Frontiers Media SA,2015©20151 online resource (108 pages) illustrations; digital, PDF file(s)Frontiers Research TopicsFrontiers in Immunology2-88919-430-2 Includes bibliographical references.Arrest chemokines are a small group of chemokines that promote leukocyte arrest from rolling by triggering rapid integrin activation. Arrest chemokines have been described for neutrophils, monocytes, eosinophils, naïve lymphocytes and effector memory T cells. Most arrest chemokines are immobilized on the endothelial surface by binding to heparan sulfate proteoglycans. Whether soluble chemokines can promote integrin activation and arrest is controversial. Many aspects of the signaling pathway from the GPCR chemokine receptor to integrin activation are the subject of active investigation. Leukocyte adhesion deficiency III is a human disease in which chemokine-triggered integrin activation is defective because of a mutation in the cytoskeletal protein kindlin-3. About 10 different such mutations have been described. The defects seen in patients with LAD-III elucidate the importance of rapid integrin activation for host defense in humans. Here we present a series of ten reports that help clarify this crucial first step in the process of leukocyte transendothelial migration.Frontiers research topics.Frontiers in immunology.ChemokinesImmunologyImmunologic diseasesImmunologychemokineLFA-1Signal TransductionTalinintegrinleukocyte adhesionVLA-4Kindlin-3ChemokinesImmunology.Immunologic diseases.Immunology.Klaus Leyauth1365936Ley Klaus1957-Frontiers Research Foundation,UkMaJRUBOOK9910137531103321Arrest chemokines3388229UNINA