Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents

This Article Full Text Full Text (PDF, 4843K) PDF+supp data (14398K) PPT slides of all figures Supplemental Material Index Alert me when this article is cited Citation Map Services Email this article Similar articles in this journal Similar articles in PubMed Alert me to new content in the JEM Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Maddaluno, L. Articles by Cavallaro, U. Search for Related Content PubMed PubMed Citation Articles by Maddaluno, L. Articles by Cavallaro, U. Social Bookmarking                            What's this?

¹ The FIRC Institute of Molecular Oncology (IFOM), 20139 Milan, Italy
² Department of Experimental Oncology, European Institute of Oncology, 20141 Milan, Italy
³ IFOM-IEO Campus, 20139 Milan, Italy
⁴ Centre for Cancer Research, Monash Institute for Medical Research, Monash University, Victoria 3800, Australia

CORRESPONDENCE Ugo Cavallaro: ugo.cavallaro{at}ifom-ieo-campus.it

The adhesion molecule L1, which is extensively characterized in the nervous system, is also expressed in dendritic cells (DCs), but its function there has remained elusive. To address this issue, we ablated L1 expression in DCs of conditional knockout mice. L1-deficient DCs were impaired in adhesion to and transmigration through monolayers of either lymphatic or blood vessel endothelial cells, implicating L1 in transendothelial migration of DCs. In agreement with these findings, L1 was expressed in cutaneous DCs that migrated to draining lymph nodes, and its ablation reduced DC trafficking in vivo. Within the skin, L1 was found in Langerhans cells but not in dermal DCs, and L1 deficiency impaired Langerhans cell migration. Under inflammatory conditions, L1 also became expressed in vascular endothelium and enhanced transmigration of DCs, likely through L1 homophilic interactions. Our results implicate L1 in the regulation of DC trafficking and shed light on novel mechanisms underlying transendothelial migration of DCs. These observations might offer novel therapeutic perspectives for the treatment of certain immunological disorders.

© 2009 Maddaluno et al.
This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.jem.org/misc/terms.shtml). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/).

CiteULike    Complore    Connotea    Del.icio.us    Digg    Facebook    Reddit    Technorati    Twitter    What's this?

This article has been cited by other articles:

• Maddaluno, L., Verbrugge, S. E., Martinoli, C., Matteoli, G., Chiavelli, A., Zeng, Y., Williams, E. D., Rescigno, M., Cavallaro, U. (2009). The adhesion molecule L1 regulates transendothelial migration and trafficking of dendritic cells. JCB 184: i14-i14 [Full Text]  

Home | Help | Feedback | Subscriptions | Archive | Search

TABLE OF CONTENTS