International Immunology Advance Access originally published online on January 12, 2006
International Immunology 2006 18(2):301-311; doi:10.1093/intimm/dxh369
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
A transmembrane chemokine, CXC chemokine ligand 16, expressed by lymph node fibroblastic reticular cells has the potential to regulate T cell migration and adhesion
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 
(TNF) and IFN
. TNF-induced expression of CXCL16 depends on NF
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-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
CiteULike 
Connotea 
Del.icio.us What's this?
This article has been cited by other articles:
|
|
 |
|
  L. Zhang, L. Ran, G. E. Garcia, X. H. Wang, S. Han, J. Du, and W. E. Mitch Chemokine CXCL16 Regulates Neutrophil and Macrophage Infiltration into Injured Muscle, Promoting Muscle Regeneration Am. J. Pathol., December 1, 2009; 175(6): 2518 - 2527. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. Barlic, W. Zhu, and P. M. Murphy Atherogenic Lipids Induce High-Density Lipoprotein Uptake and Cholesterol Efflux in Human Macrophages by Up-Regulating Transmembrane Chemokine CXCL16 without Engaging CXCL16-Dependent Cell Adhesion J. Immunol., June 15, 2009; 182(12): 7928 - 7936. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. Suto, T. Katakai, M. Sugai, T. Kinashi, and A. Shimizu CXCL13 production by an established lymph node stromal cell line via lymphotoxin-beta receptor engagement involves the cooperation of multiple signaling pathways Int. Immunol., April 1, 2009; 21(4): 467 - 476. [Abstract] [Full Text] [PDF]
|
|