趋化因子受体最早是在研究白细胞迁移过程中发现的，它在大鼠和小鼠的背根神经节外周感觉神经细胞上也有表达.在炎症情况下，激活的趋化因子受体可以诱导神经细胞上一类重要的镇痛受体—μ-鸦片受体的异源性脱敏，抑制其功能；同时，激活的趋化因子受体还可以增强一类对于痛觉感受非常关键的受体——辣椒素受体的敏感性，使其敏化.趋化因子受体诱导的这2种效应可以通过Gi蛋白信号传导通路增强生物体对痛觉的敏感度.这些结果提示，趋化因子受体可能是免疫系统和神经系统之间交叉调节的桥梁.

Chemokine receptors, originally discovered to mediate leukocytes trafficking, were detected on peripheral sensory neurons in the dorsal root ganglia of rats and mice.Upon activation, these receptors mediate chemokineinduced heterologous desensitization of μ-opioid receptors, a class of key analgesic receptors on neurons.Furthermore, chemokine treatment also enhances the sensitivity of transient receptor potential vanilloid 1 (TRPV1), a heat-and ligand-gated calcium channel that is critical for sensing pain. During inflammation, activation of chemokine receptors on neurons contributes to hyperalgesia by inhibitingμ-opioid receptors and concomitantly sensitizing TRPV1, via Gi-protein mediated signaling pathways. Thus,based on above analysis, we proposed that chemokine receptors may serve as a linkage between the immune and neural systems.