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Prepublished online as a Blood First Edition Paper on May 24, 2002; DOI 10.1182/blood-2002-01-0260.
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Blood, 15 September 2002, Vol. 100, No. 6, pp. 1948-1956
CHEMOKINES
CCL19 induces rapid dendritic extension of murine dendritic
cells
Yoshiki Yanagawa and
Kazunori Onoé
From the Division of Immunobiology, Institute for
Genetic Medicine, Hokkaido University, Sapporo, Japan.
Dendritic cells (DCs) 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 a 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 DCs, but not immature DCs, showed vigorous migration
to either CCL19 or CCL21. CCL19 also rapidly (within 30 minutes)
induced marked extension of dendrites of mature DCs 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
DCs, 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 DCs. The CCL19-induced morphologic
changes were completely blocked by Clostridium difficile
toxin B that inhibits Rho guanosine triphosphatase proteins such as
Rho, Rac, and Cdc42, but not by Y-27632, a specific inhibitor for
Rho-associated kinase. These findings suggest that Rac or Cdc42 (or
both), but not Rho, are involved in the CCL19-induced dendritic
extension of mature DCs.

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