{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2023,10,30]],"date-time":"2023-10-30T09:59:11Z","timestamp":1698659951114},"reference-count":30,"publisher":"Rockefeller University Press","issue":"12","content-domain":{"domain":["rupress.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[1998,6,15]]},"abstract":"<jats:p>L1 is an immunoglobulin superfamily adhesion molecule highly expressed on neurons and involved in cell motility, neurite outgrowth, axon fasciculation, myelination, and synaptic plasticity. L1 is also expressed by nonneural cells, but its function outside of the nervous system has not been studied extensively. We find that administration of an L1 monoclonal antibody in vivo disrupts the normal remodeling of lymph node reticular matrix during an immune response. Ultrastructural examination reveals that reticular fibroblasts in mice treated with L1 monoclonal antibodies fail to spread and envelop collagen fibers with their cellular processes. The induced defect in the remodeling of the fibroblastic reticular system results in the loss of normal nodal architecture, collapsed cortical sinusoids, and macrophage accumulation in malformed sinuses. Surprisingly, such profound architectural abnormalities have no detectable effects on the primary immune response to protein antigens.<\/jats:p>","DOI":"10.1084\/jem.187.12.1953","type":"journal-article","created":{"date-parts":[[2002,7,26]],"date-time":"2002-07-26T16:49:30Z","timestamp":1027702170000},"page":"1953-1963","update-policy":"http:\/\/dx.doi.org\/10.1084\/jem.crossmarkpolicy","source":"Crossref","is-referenced-by-count":19,"title":["L1 Antibodies Block Lymph Node Fibroblastic Reticular Matrix Remodeling In Vivo"],"prefix":"10.1084","volume":"187","author":[{"given":"Gino","family":"Di Sciullo","sequence":"first","affiliation":[{"name":"From the *Department of Pathology and Laboratory Medicine, Boston University School of Medicine, Boston, Massachusetts 02118; the \u2021Department of Neurobiology, Swiss Federal Institute of Technology, CH-8093 Zurich, Switzerland; and \u00a7Zentrum f\u00fcr Molekulare Neurobiologie, Universit\u00e4t Hamburg, D-20246 Hamburg, Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Tim","family":"Donahue","sequence":"additional","affiliation":[{"name":"From the *Department of Pathology and Laboratory Medicine, Boston University School of Medicine, Boston, Massachusetts 02118; the \u2021Department of Neurobiology, Swiss Federal Institute of Technology, CH-8093 Zurich, Switzerland; and \u00a7Zentrum f\u00fcr Molekulare Neurobiologie, Universit\u00e4t Hamburg, D-20246 Hamburg, Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Melitta","family":"Schachner","sequence":"additional","affiliation":[{"name":"From the *Department of Pathology and Laboratory Medicine, Boston University School of Medicine, Boston, Massachusetts 02118; the \u2021Department of Neurobiology, Swiss Federal Institute of Technology, CH-8093 Zurich, Switzerland; and \u00a7Zentrum f\u00fcr Molekulare Neurobiologie, Universit\u00e4t Hamburg, D-20246 Hamburg, Germany"},{"name":"From the *Department of Pathology and Laboratory Medicine, Boston University School of Medicine, Boston, Massachusetts 02118; the \u2021Department of Neurobiology, Swiss Federal Institute of Technology, CH-8093 Zurich, Switzerland; and \u00a7Zentrum f\u00fcr Molekulare Neurobiologie, Universit\u00e4t Hamburg, D-20246 Hamburg, Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Steven A.","family":"Bogen","sequence":"additional","affiliation":[{"name":"From the *Department of Pathology and Laboratory Medicine, Boston University School of Medicine, Boston, Massachusetts 02118; the \u2021Department of Neurobiology, Swiss Federal Institute of Technology, CH-8093 Zurich, Switzerland; and \u00a7Zentrum f\u00fcr Molekulare Neurobiologie, Universit\u00e4t Hamburg, D-20246 Hamburg, 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