TY - JOUR
T1 - Cutting edge
T2 - Critical role of CXCL16/CXCR6 in NKT cell trafficking in allograft tolerance
AU - Jiang, Xiaofeng
AU - Shimaoka, Takeshi
AU - Kojo, Satoshi
AU - Harada, Michishige
AU - Watarai, Hiroshi
AU - Wakao, Hiroshi
AU - Ohkohchi, Nobuhiro
AU - Yonehara, Shin
AU - Taniguchi, Masaru
AU - Seino, Ken Ichiro
PY - 2005/8/15
Y1 - 2005/8/15
N2 - It is well-documented that certain chemokines or their receptors play important roles in the graft rejection. However, the roles of chemokines and their receptors in the maintenance of transplantation tolerance remain unclear. In this study, we demonstrate that blocking of the interaction between the chemokine receptor, CXCR6, highly expressed on Vα14+ NKT cells and its ligand, CXCL16, resulted in the failure to maintain graft tolerance and thus in the induction of acceleration of graft rejection. In a mouse transplant tolerance model, the expression of CXCL16 was up-regulated in the tolerated allografts, and anti-CXCL16 mAb inhibited intragraft accumulation of NKT cells. In vitro experiments farther showed that blocking of CXCL16/CXCR6 interaction significantly affected not only chemotaxis but also cell adhesion of NKT cells. These results demonstrate the unique role of CXCL16 and CXCR6 molecules in the maintenance of cardiac allograft tolerance mediated by NKT cells.
AB - It is well-documented that certain chemokines or their receptors play important roles in the graft rejection. However, the roles of chemokines and their receptors in the maintenance of transplantation tolerance remain unclear. In this study, we demonstrate that blocking of the interaction between the chemokine receptor, CXCR6, highly expressed on Vα14+ NKT cells and its ligand, CXCL16, resulted in the failure to maintain graft tolerance and thus in the induction of acceleration of graft rejection. In a mouse transplant tolerance model, the expression of CXCL16 was up-regulated in the tolerated allografts, and anti-CXCL16 mAb inhibited intragraft accumulation of NKT cells. In vitro experiments farther showed that blocking of CXCL16/CXCR6 interaction significantly affected not only chemotaxis but also cell adhesion of NKT cells. These results demonstrate the unique role of CXCL16 and CXCR6 molecules in the maintenance of cardiac allograft tolerance mediated by NKT cells.
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U2 - 10.4049/jimmunol.175.4.2051
DO - 10.4049/jimmunol.175.4.2051
M3 - Article
C2 - 16081769
AN - SCOPUS:23444444682
VL - 175
SP - 2051
EP - 2055
JO - Journal of Immunology
JF - Journal of Immunology
SN - 0022-1767
IS - 4
ER -