{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,4]],"date-time":"2026-10-04T04:29:02Z","timestamp":1791088142985,"version":"4.1.0"},"reference-count":59,"publisher":"Oxford University Press (OUP)","issue":"9","license":[{"start":{"date-parts":[[2003,5,1]],"date-time":"2003-05-01T00:00:00Z","timestamp":1051747200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2003,5,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Naive T cells are usually excluded from nonlymphoid tissues. Only when such tertiary tissues are subjected to chronic inflammation, such as in some (but not all) autoimmune diseases, are naive T cells recruited to these sites. We show that the CCR7 ligand CC chemokine ligand (CCL)21 is sufficient for attracting naive T cells into tertiary organs. We performed intravital microscopy of cremaster muscle venules in T-GFP mice, in which naive T cells express green fluorescent protein (GFP). GFP+ cells underwent selectin-dependent rolling, but no firm adherence (sticking). Superfusion with CCL21, but not CXC chemokine ligand 12, induced integrin-dependent sticking of GFP+ cells. Moreover, CCL21 rapidly elicited accumulation of naive T cells into sterile s.c. air pouches. Interestingly, a second CCR7 ligand, CCL19, triggered T cell sticking in cremaster muscle venules, but failed to induce extravasation in air pouches. Immunohistochemistry studies implicate ectopic expression of CCL21 as a mechanism for naive T cell traffic in human autoimmune diseases. Most blood vessels in tissue samples from patients with rheumatoid arthritis (85 \u00b1 10%) and ulcerative colitis (66 \u00b1 1%) expressed CCL21, and many perivascular CD45RA+ naive T cells were found in these tissues, but not in psoriasis, where CCL21+ vessels were rare (17 \u00b1 1%). These results identify endothelial CCL21 expression as an important determinant for naive T cell migration to tertiary tissues, and suggest the CCL21\/CCR7 pathway as a therapeutic target in diseases that are associated with naive T cell recruitment.<\/jats:p>","DOI":"10.4049\/jimmunol.170.9.4638","type":"journal-article","created":{"date-parts":[[2014,4,20]],"date-time":"2014-04-20T18:18:42Z","timestamp":1398017922000},"page":"4638-4648","source":"Crossref","is-referenced-by-count":159,"title":["Naive T Cell Recruitment to Nonlymphoid Tissues: A Role for Endothelium-Expressed CC Chemokine Ligand 21 in Autoimmune Disease and Lymphoid Neogenesis"],"prefix":"10.1093","volume":"170","author":[{"given":"Wolfgang","family":"Weninger","sequence":"first","affiliation":[{"name":"The Center for Blood Research and Department of Pathology, Harvard Medical School , Boston, MA 02115"},{"name":"Department of Pathology, Harvard Medical School , Boston, MA 02115"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hege S","family":"Carlsen","sequence":"additional","affiliation":[{"name":"Institute of Pathology and Department of Surgery, University of Oslo , Rikshospitalet ,","place":["Norway"]},{"name":"Department of Surgery, University of Oslo , Rikshospitalet ,","place":["Norway"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mahmoud","family":"Goodarzi","sequence":"additional","affiliation":[{"name":"The Center for Blood Research and Department of Pathology, Harvard Medical School , Boston, MA 02115"},{"name":"Department of Pathology, Harvard Medical School , Boston, MA 02115"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Farzad","family":"Moazed","sequence":"additional","affiliation":[{"name":"The Center for Blood Research and Department of Pathology, Harvard Medical School , Boston, MA 02115"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Maura A","family":"Crowley","sequence":"additional","affiliation":[{"name":"The Center for Blood Research and Department of Pathology, Harvard Medical School , Boston, MA 02115"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Espen S","family":"Baekkevold","sequence":"additional","affiliation":[{"name":"Institute of Pathology and Department of Surgery, University of Oslo , Rikshospitalet ,","place":["Norway"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lois L","family":"Cavanagh","sequence":"additional","affiliation":[{"name":"The Center for Blood Research and Department of Pathology, Harvard Medical School , Boston, MA 02115"},{"name":"Department of Pathology, Harvard Medical School , Boston, MA 02115"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ulrich H","family":"von Andrian","sequence":"additional","affiliation":[{"name":"The Center for Blood Research and Department of Pathology, Harvard Medical School , Boston, MA 02115"},{"name":"Department of Pathology, Harvard Medical School , Boston, MA 02115"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2003,5,1]]},"reference":[{"key":"2026020210070372300_R1","first-page":"60","volume-title":"Science","year":"1996"},{"key":"2026020210070372300_R2","first-page":"1020","volume-title":"N. 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