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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.
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Submitted January 12, 2005
Accepted May 22, 2005
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
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
Institute of Molecular and Cellular Biosciences, The University of Tokyo, Tokyo, Japan
* Corresponding author; email: tanaka{at}orgctl.med.osaka-u.ac.jp.
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's patches (PPs), serves as an arrest chemokine for B cells. Whole-mount analysis of mesenteric LNs (MLNs) showed that, unlike T cells, B cells adhere poorly to the HEVs of CXCL13-/- mice and that B-cell adhesion is substantially restored in CXCL13-/- HEVs when CXCL13 was added to the MLNs by superfusion, as we have previously observed in PP HEVs by intravital microscopy. In vitro, CXCL13 activated the small 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.
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