{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T13:01:39Z","timestamp":1791291699011,"version":"4.1.0"},"reference-count":40,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2012,9,4]],"date-time":"2012-09-04T00:00:00Z","timestamp":1346716800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Immunology"],"published-print":{"date-parts":[[2012,10]]},"abstract":"Summary<\/jats:title>\n \n T\u2010cell scanning for antigen\u2010presenting cells (\n APC<\/jats:styled-content>\n ) is a finely tuned process. Whereas non\u2010cognate\n APC<\/jats:styled-content>\n trigger\n T<\/jats:styled-content>\n \u2010cell motility via chemokines and intercellular adhesion molecule\u20101 (\n ICAM<\/jats:styled-content>\n \u20101), cognate\n APC<\/jats:styled-content>\n deliver a stop signal resulting from antigen recognition. We tested\n in vitro<\/jats:italic>\n the contribution of the actin cytoskeleton regulator\n W<\/jats:styled-content>\n iskott\u2013\n A<\/jats:styled-content>\n ldrich syndrome protein (\n WASP<\/jats:styled-content>\n ) to the scanning activity of primary human\n CD<\/jats:styled-content>\n 4\n +<\/jats:sup>\n \u00a0\n T<\/jats:styled-content>\n cells.\n WASP<\/jats:styled-content>\n knock\u2010down resulted in increased\n T<\/jats:styled-content>\n \u2010cell motility upon encounter with non\u2010cognate dendritic cells or\n B<\/jats:styled-content>\n cells and reduced capacity to stop following antigen recognition. The high motility of\n WASP<\/jats:styled-content>\n \u2010deficient\n T<\/jats:styled-content>\n cells was accompanied by a diminished ability to round up and to stabilize pauses.\n WASP<\/jats:styled-content>\n \u2010deficient T cells migrated in a normal proportion towards\n CXCL<\/jats:styled-content>\n 12,\n CCL<\/jats:styled-content>\n 19 and\n CCL<\/jats:styled-content>\n 21, but displayed an increased adhesion and elongation on\n ICAM<\/jats:styled-content>\n \u20101. The elongated morphology of\n WASP<\/jats:styled-content>\n \u2010deficient\n T<\/jats:styled-content>\n cells was related to a reduced confinement of high\u2010affinity lymphocyte function\u2010associated antigen 1 to the mid\u2010cell zone. Our data therefore indicate that\n WASP<\/jats:styled-content>\n controls\n CD<\/jats:styled-content>\n 4\n +<\/jats:sup>\n T\u2010cell motility upon\n APC<\/jats:styled-content>\n encounter by regulating lymphocyte function\u2010associated antigen 1 spatial distribution.\n <\/jats:p>","DOI":"10.1111\/j.1365-2567.2012.03620.x","type":"journal-article","created":{"date-parts":[[2012,7,19]],"date-time":"2012-07-19T02:57:43Z","timestamp":1342666663000},"page":"183-196","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":30,"title":["W<\/scp>\n iskott\u2013\n A<\/scp>\n ldrich syndrome protein controls antigen\u2010presenting cell\u2010driven\n CD<\/scp>\n 4\n +<\/sup>\n T\u2010cell motility by regulating adhesion to intercellular adhesion molecule\u20101"],"prefix":"10.1111","volume":"137","author":[{"given":"Fanny","family":"Lafouresse","sequence":"first","affiliation":[{"name":"INSERM U1043 Toulouse 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