Department of Surgery, the Fourth Affiliated Hospital, China Medical University, Shengyang, 110032, China.
Transpl Immunol. 2010 Feb;22(3-4):179-83. doi: 10.1016/j.trim.2009.12.001. Epub 2009 Dec 24.
CXCL16/SR-PSOX is a novel transmembrane-type chemokine, which was also identified as a novel scavenger receptor for oxidized low density lipoprotein. Its receptor CXCR6 expresses on activated CD8(+) T cells, type 1-polarized CD4(+), and constitutively expresses on NKT cells. Moreover, it has been shown that CXCL16 accumulated activated CD8(+) T cells to sites of inflammation. To date, the effect of CXCL16 (SR-PSOX)/CXCR6 on CD8(+) T cells and its role in allograft rejection/acceptance are not well understood. In the current study, we show that rejected allografts showed higher expressions of CXCR6 and CXCL16. More importantly, expression of CXCR6 on CD8(+) T cells was also up-regulated by rejection. However, the blockade of CXCL16(SR-PSOX)/CXCR6 interaction could not inhibit cytotoxic activity of CD8(+) T cells, and therefore, could not prolong the cardiac graft survival time.
趋化因子（C-X-C 基元）配体 16/信号调节蛋白 X 连锁（SR-PSOX）是一种新型的跨膜型趋化因子，也被鉴定为氧化型低密度脂蛋白的新型清道夫受体。其受体 CXCR6 表达于活化的 CD8(+)T 细胞、1 型极化的 CD4(+)和自然杀伤 T 细胞上。此外，已经表明趋化因子（C-X-C 基元）配体 16/信号调节蛋白 X 连锁（SR-PSOX）募集活化的 CD8(+)T 细胞至炎症部位。迄今为止，趋化因子（C-X-C 基元）配体 16/信号调节蛋白 X 连锁（SR-PSOX）（CXCR6）对 CD8(+)T 细胞的影响及其在同种异体移植物排斥/接受中的作用尚不清楚。在本研究中，我们表明，被排斥的同种异体移植物显示出更高的 CXCR6 和趋化因子（C-X-C 基元）配体 16 的表达。更重要的是，排斥也上调了 CD8(+)T 细胞上的 CXCR6 表达。然而，阻断趋化因子（C-X-C 基元）配体 16/信号调节蛋白 X 连锁（SR-PSOX）/CXCR6 相互作用不能抑制 CD8(+)T 细胞的细胞毒性活性，因此不能延长心脏移植物的存活时间。
