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Prepublished online as a Blood First Edition Paper on May 24, 2002; DOI 10.1182/blood-2002-01-0260. This Article Full Text (PDF) All Versions of this Article: 2002-01-0260v1 100/6/1948    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Yanagawa, Y. Articles by Onoe, K. Search for Related Content PubMed PubMed Citation Articles by Yanagawa, Y. Articles by Onoe, K. Social Bookmarking                   What's this? Submitted February 13, 2002 Accepted May 2, 2002 CCL19 induces rapid dendritic extension of murine dendritic cells Yoshiki Yanagawa and Kazunori Onoe* Institute for Genetic Medicine, Hokkaido University, Sapporo, Japan * Corresponding author; email: kazunori{at}imm.hokudai.ac.jp. Dendritic cells (DC) possess numerous dendrites that may be of great advantage to interaction with T cells. However, it has been poorly understood how the dendritic morphology of DC is controlled. In the present study, using a murine spleen-derived DC line, we analyzed effects of CCR7-ligands, CCL19 and CCL21, on dendritic morphology. Mature DC, but not immature, showed vigorous migration to either CCL19 or CCL21. CCL19 also rapidly (within 30 minutes) induced marked extension of dendrites of mature DC that was maintained at least for 24 hours. On the other hand, CCL21 failed to induce rapid dendritic extension, even though a modest dendritic extension of mature DC, compared to that by CCL19, was induced 8 or 24 hours after treatment with CCL21. In addition, pretreatment with a high concentration of CCL21 significantly inhibited the rapid dendritic extension induced by CCL19. Thus, it is suggested that CCL19 and CCL21 exert agonistic and antagonistic influences on the initiation of dendritic extension of mature DC. The CCL19-induced morphological changes were completely blocked by Clostridium difficile toxin B that inhibits Rho GTPase proteins such as Rho, Rac and Cdc42, but not by Y-27632, a specific inhibitor for Rho-associated kinase. These findings suggest that that Rac and/or Cdc42, but not Rho, are involved in the CCL19-induced dendritic extension of mature DC. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: C. Escribano, C. 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