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Blood, 15 October 2005, Vol. 106, No. 8, pp. 2613-2618. Prepublished online as a Blood First Edition Paper on June 21, 2005; DOI 10.1182/blood-2005-01-0133. This Article Full Text Full Text (PDF) All Versions of this Article: 2005-01-0133v1 106/8/2613    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 Kanemitsu, N. Articles by Miyasaka, M. Search for Related Content PubMed PubMed Citation Articles by Kanemitsu, N. Articles by Miyasaka, M. Related Collections Hemostasis, Thrombosis, and Vascular Biology Immunobiology Chemokines, Cytokines, and Interleukins Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  CHEMOKINES, CYTOKINES, AND INTERLEUKINS CXCL13 is an arrest chemokine for B cells in high endothelial venules Naotoshi Kanemitsu, Yukihiko Ebisuno, Toshiyuki Tanaka, Kazuhiro Otani, Haruko Hayasaka, Tsuneyasu Kaisho, Shizuo Akira, Koko Katagiri, Tatsuo Kinashi, Naoya Fujita, Takashi Tsuruo, and Masayuki Miyasaka From the Laboratory of Immunodynamics, Department of Microbiology and Immunology, Osaka University Graduate School of Medicine, Osaka, Japan; Research Center for Allergy and Immunology, the Institute of Physical and Chemical Research (RIKEN), Kanagawa, Japan; Research Institute for Microbial Diseases, Osaka University, Osaka, Japan; Department of Molecular Genetics, Kansai Medical University, Osaka, Japan; and the Institute of Molecular and Cellular Biosciences, University of Tokyo, Tokyo, Japan. Chemokine receptor signaling is critical for lymphocyte trafficking across high endothelial venules (HEVs), but the exact mode of action of individual chemokines expressed in the HEVs is unclear. Here we report that CXCL13, expressed in a substantial proportion of HEVs in both lymph nodes (LNs) and Peyer patches (PPs), serves as an arrest chemokine for B cells. Whole-mount analysis of mesenteric LNs (MLNs) showed that, unlike T cells, B cellsa dhere poorly to the HEVs of CXCL13–/– mice and that B-cell adhesion is substantially restored in CXCL13–/– HEVs when CXCL13 is added to the MLNs by superfusion, as we have previously observed in PP HEVs by intravital microscopy. In vitro, CXCL13 activated the small guanosine triphosphatase (GTPase) Rap1 in B cells, and corroborating this observation, a deficiency of RAPL, the Rap1 effector molecule, caused a significant reduction in shear-resistant B-cell adhesion to intercellular adhesion molecule 1 (ICAM-1). In addition, CXCL13 induced B-cell adhesion to mucosal addressin cell adhesion molecule 1 (MAdCAM-1) by activating 4 integrin. These data identify CXCL13 as an arrest chemokine for B cells in HEVs and show that CXCL13 plays an important role in B-cell entry into not only PPs but also MLNs. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: Y. Chen, M. Yu, A. Podd, R. Wen, M. Chrzanowska-Wodnicka, G. C. White, and D. Wang A critical role of Rap1b in B-cell trafficking and marginal zone B-cell development Blood, May 1, 2008; 111(9): 4627 - 4636. [Abstract] [Full Text] [PDF] J. L. Hermsen, F. E. Gomez, Y. Maeshima, Y. Sano, W. Kang, and K. A. Kudsk Decreased Enteral Stimulation Alters Mucosal Immune Chemokines JPEN J Parenter Enteral Nutr, January 1, 2008; 32(1): 36 - 44. [Abstract] [Full Text] [PDF] A. Burkle, M. Niedermeier, A. Schmitt-Graff, W. G. Wierda, M. J. Keating, and J. A. Burger Overexpression of the CXCR5 chemokine receptor, and its ligand, CXCL13 in B-cell chronic lymphocytic leukemia Blood, November 1, 2007; 110(9): 3316 - 3325. [Abstract] [Full Text] [PDF]

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