{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T20:33:32Z","timestamp":1791318812675,"version":"4.3.1"},"reference-count":0,"publisher":"Rockefeller University Press","issue":"6","content-domain":{"domain":["rupress.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[1995,6,1]]},"abstract":"<jats:p>L-selectin, a cell surface adhesion molecule that is expressed by most leukocytes, mediates leukocyte rolling along vascular endothelium at sites of inflammation. The contribution of L-selectin to leukocyte migration in models of chronic inflammation was assessed by using mice that lack cell surface L-selectin expression. Significant inhibition of neutrophil (56-62%), lymphocyte (70-75%), and monocyte (72-78%) migration into an inflamed peritoneum was observed 24 and 48 h after administration of thioglycollate, an inflammatory stimulus. L-selectin-deficient mice were also significantly impaired in delayed-type hypersensitivity reactions. Footpad swelling in response to sheep red blood cell challenge was reduced 75% in L-selectin-deficient mice compared with wild-type mice. Ear swelling in a model of contact hypersensitivity induced by oxazolone challenge was also reduced by 69% compared to wild-type mice. Consistent with L-selectin-mediating leukocyte migration into diverse vascular beds during inflammation, L-selectin-deficient mice were significantly resistant to death resulting from lipopolysaccharide (LPS)-induced toxic shock. LPS administration resulted in a 90% mortality rate in control mice after 24 h, while there was a 90% survival rate in L-selectin-deficient mice. These results demonstrate that L-selectin plays a prominent role in leukocyte homing to nonlymphoid tissues during inflammation and that blocking this process can be beneficial during pathological inflammatory responses.<\/jats:p>","DOI":"10.1084\/jem.181.6.2259","type":"journal-article","created":{"date-parts":[[2004,6,24]],"date-time":"2004-06-24T07:56:10Z","timestamp":1088063770000},"page":"2259-2264","update-policy":"https:\/\/doi.org\/10.1084\/jem.crossmarkpolicy","source":"Crossref","is-referenced-by-count":327,"title":["L-selectin-deficient mice have impaired leukocyte recruitment into inflammatory sites."],"prefix":"10.1084","volume":"181","author":[{"given":"T F","family":"Tedder","sequence":"first","affiliation":[{"name":"Department of Immunology, Duke University Medical Center, Durham, North Carolina 27710, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"D A","family":"Steeber","sequence":"additional","affiliation":[{"name":"Department of Immunology, Duke University Medical Center, Durham, North Carolina 27710, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"P","family":"Pizcueta","sequence":"additional","affiliation":[{"name":"Department of Immunology, Duke University Medical Center, Durham, North Carolina 27710, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"291","published-online":{"date-parts":[[1995,6,1]]},"container-title":["The Journal of experimental medicine"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/rupress.org\/jem\/article-pdf\/181\/6\/2259\/1677264\/2259.pdf","content-type":"application\/pdf","content-version":"vor","intended-application":"syndication"},{"URL":"https:\/\/rupress.org\/jem\/article-pdf\/181\/6\/2259\/1677264\/2259.pdf","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2023,7,25]],"date-time":"2023-07-25T06:52:04Z","timestamp":1690267924000},"score":1,"resource":{"primary":{"URL":"https:\/\/rupress.org\/jem\/article\/181\/6\/2259\/57583\/L-selectin-deficient-mice-have-impaired-leukocyte"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[1995,6,1]]},"references-count":0,"journal-issue":{"issue":"6","published-print":{"date-parts":[[1995,6,1]]}},"URL":"https:\/\/doi.org\/10.1084\/jem.181.6.2259","relation":{},"ISSN":["0022-1007","1540-9538"],"issn-type":[{"value":"0022-1007","type":"print"},{"value":"1540-9538","type":"electronic"}],"subject":[],"published":{"date-parts":[[1995,6,1]]}}}