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Blood, 15 March 2008, Vol. 111, No. 6, pp. 2973-2976. Prepublished online as a Blood First Edition Paper on January 15, 2008; DOI 10.1182/blood-2007-09-112169. This Article Full Text Full Text (PDF) Supplemental Table All Versions of this Article: blood-2007-09-112169v1 111/6/2973    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map 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 Gotoh, K. Articles by Fukui, Y. Search for Related Content PubMed PubMed Citation Articles by Gotoh, K. Articles by Fukui, Y. Related Collections Brief Reports Chemokines, Cytokines, and Interleukins Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  CHEMOKINES, CYTOKINES, AND INTERLEUKINS Brief Report Differential requirement for DOCK2 in migration of plasmacytoid dendritic cells versus myeloid dendritic cells Kazuhito Gotoh1,2, Yoshihiko Tanaka1, Akihiko Nishikimi1, Ayumi Inayoshi1, Munechika Enjoji2, Ryoichi Takayanagi2, Takehiko Sasazuki3, and Yoshinori Fukui1 1 Division of Immunogenetics, Department of Immunobiology and Neuroscience, Medical Institute of Bioregulation, Kyushu University, Fukuoka; 2 Department of Medicine and Bioregulatory Science, Graduate School of Medical Sciences, Kyushu University, Fukuoka; and 3 International Medical Center of Japan, Tokyo, Japan The migratory properties of dendritic cells (DCs) are important for their functions. Although several chemokines and their receptors have been implicated in DC migration, the downstream signaling molecules are largely unknown. Here we show that DOCK2, a hematopoietic cell-specific CDM family protein, is indispensable for migration of plasmacytoid DCs (pDCs), but not myeloid DCs (mDCs). Although DOCK2-deficiency did not affect development of pDCs, DOCK2-deficient (DOCK2–/–) mice exhibited a severe reduction of pDCs in the spleen and lymph nodes. Adoptive transfer experiments revealed that DOCK2–/– pDCs failed to migrate into the periarteriolar lymphoid sheaths of the spleen. In DOCK2–/– pDCs, chemokine-induced Rac activation was severely impaired, resulting in the reduction of motility and the loss of polarity during chemotaxis. In contrast, DOCK2–/– mDCs did not show any defects in Rac activation and migration. These results indicate that pDCs and mDCs use distinct molecules to activate Rac during chemotaxis. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: P. J. Cimino, I. Sokal, J. Leverenz, Y. Fukui, and T. J. Montine DOCK2 Is a Microglial Specific Regulator of Central Nervous System Innate Immunity Found in Normal and Alzheimer's Disease Brain Am. J. Pathol., October 1, 2009; 175(4): 1622 - 1630. [Abstract] [Full Text] [PDF]

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