Skip Navigation


International Immunology Advance Access originally published online on January 12, 2006
International Immunology 2006 18(2):301-311; doi:10.1093/intimm/dxh369
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow All Versions of this Article:
18/2/301    most recent
dxh369v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (5)
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Hara, T.
Right arrow Articles by Shimizu, A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Hara, T.
Right arrow Articles by Shimizu, A.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?


© The Japanese Society for Immunology. 2006. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org

A transmembrane chemokine, CXC chemokine ligand 16, expressed by lymph node fibroblastic reticular cells has the potential to regulate T cell migration and adhesion

Takahiro Hara1,2, Tomoya Katakai1,4, Jong-Hwan Lee1,2, Yukiko Nambu1,2, Natsuki Nakajima-Nagata1, Hiroyuki Gonda1,3, Manabu Sugai1 and Akira Shimizu1,2,3

1 Center for Genomic Medicine, Graduate School of Medicine and 2 Division of Systemic Life Sciences, Graduate School of Biostudies, Kyoto University, Kyoto, Japan
3 Translational Research Center, Kyoto University Hospital, Kyoto 606-8507, Japan
4 Present address: 53 Shogoin-Kawahara-cho, Sakyo-ku, Kyoto 606-8507, Japan

Correspondence to: T. Katakai; E-mail: tkatakai{at}virus.kyoto-u.ac.jp

Stromal cells in lymphoid tissues provide microenvironmental fields required for the triggering of efficient immune responses. Fibroblastic reticular cells (FRCs) are one of the integral constituents of such stromal fields; they construct the reticular network and are considered to regulate immune cells' behavior. However, the factors that mediate the interaction between lymphocytes and FRCs are poorly understood. Here we show that a mouse lymph node (LN)-derived FRC cell line, BLS4, expresses a transmembrane chemokine, CXC chemokine ligand (CXCL) 16, in response to tumor necrosis factor {alpha} (TNF{alpha}) and IFN{gamma}. TNF{alpha}-induced expression of CXCL16 depends on NF{kappa}B, p38 MAPK and PKA. Matrix metalloproteinase activity is required for producing soluble CXCL16 in the culture supernatant, likely via shedding at the juxtamembrane region of the extracellular domain. IL-12 enhances the expression of CXCR6 in anti-CD3/CD28-stimulated CD8+ T cells and their adhesion to the BLS4 cell surface in a TNF{alpha}-dependent fashion. The adherence is significantly inhibited in the presence of both anti-CXCL16 and anti-vascular cell adhesion molecule 1 (VCAM-1) antibodies. CXCL16 expression is also detected in the FRCs in LN sections and in gp38+VCAM-1+ FRCs isolated from LNs. Taken together, these findings suggest that CXCL16 is an important mediator of lymphocyte–stromal interaction within lymphoid tissues.

Keywords: chemotaxis, CXCR6, inflammatory cytokines, lymphocytes, stromal cells

Transmitting editor: T. Watanabe


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?




Disclaimer:
Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.