LEADER 00963cam0-22003611i-450- 001 990007029620403321 005 20070704112952.0 010 $a88-15-07913-0 035 $a000702962 035 $aFED01000702962 035 $a(Aleph)000702962FED01 035 $a000702962 100 $a20020115d2001----km-y0itay50------ba 101 0 $aita 102 $aIT 105 $ay-------001yb 200 1 $aEnrico Mattei$fNico Perrone 210 $aBologna$cIl mulino$d2001 215 $a167 p.$d21 cm 225 1 $a<>identità italiana$v22 610 0 $aMattei, Enrico 610 0 $aMattei, Enrico 676 $a338.76655092$v21$zita 700 1$aPerrone,$bNico$f<1935- >$0141827 801 0$aIT$bUNINA$gRICA$2UNIMARC 901 $aBK 912 $a990007029620403321 952 $aCollez. 1821 (22)$b37236$fFSPBC 952 $a338.76 MAT 1$bBibl.41479$fFLFBC 959 $aFSPBC 959 $aFLFBC 996 $aEnrico Mattei$9509235 997 $aUNINA LEADER 02781nam 2200565 450 001 9910137531103321 005 20230621135640.0 035 $a(CKB)3710000000569674 035 $a(oapen)https://directory.doabooks.org/handle/20.500.12854/41301 035 $a(EXLCZ)993710000000569674 100 $a20160125h20152015 fy| 0 101 0 $aeng 135 $aurmu#---uuuuu 181 $ctxt$2rdacontent 182 $cc$2rdamedia 183 $acr$2rdacarrier 200 00$aArrest chemokines$b[electronic resource] /$ftopic editor: Klaus Ley 210 $cFrontiers Media SA$d2015 210 1$a[Lausanne, Switzerland] :$cFrontiers Media SA,$d2015 210 4$d©2015 215 $a1 online resource (108 pages) $cillustrations; digital, PDF file(s) 225 1 $aFrontiers Research Topics 225 1 $aFrontiers in Immunology 311 $a2-88919-430-2 320 $aIncludes bibliographical references. 330 3 $aArrest chemokines are a small group of chemokines that promote leukocyte arrest from rolling by triggering rapid integrin activation. Arrest chemokines have been described for neutrophils, monocytes, eosinophils, naïve lymphocytes and effector memory T cells. Most arrest chemokines are immobilized on the endothelial surface by binding to heparan sulfate proteoglycans. Whether soluble chemokines can promote integrin activation and arrest is controversial. Many aspects of the signaling pathway from the GPCR chemokine receptor to integrin activation are the subject of active investigation. Leukocyte adhesion deficiency III is a human disease in which chemokine-triggered integrin activation is defective because of a mutation in the cytoskeletal protein kindlin-3. About 10 different such mutations have been described. The defects seen in patients with LAD-III elucidate the importance of rapid integrin activation for host defense in humans. Here we present a series of ten reports that help clarify this crucial first step in the process of leukocyte transendothelial migration. 410 0$aFrontiers research topics. 410 0$aFrontiers in immunology. 606 $aChemokines$xImmunology 606 $aImmunologic diseases 606 $aImmunology 610 $achemokine 610 $aLFA-1 610 $aSignal Transduction 610 $aTalin 610 $aintegrin 610 $aleukocyte adhesion 610 $aVLA-4 610 $aKindlin-3 615 0$aChemokines$xImmunology. 615 0$aImmunologic diseases. 615 0$aImmunology. 700 $aKlaus Ley$4auth$01365936 702 $aLey$b Klaus$f1957- 712 02$aFrontiers Research Foundation, 801 2$bUkMaJRU 906 $aBOOK 912 $a9910137531103321 996 $aArrest chemokines$93388229 997 $aUNINA