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免疫调节因子白细胞介素-2(IL-2)具有中枢镇痛功能。实验采用基因定位突变技术,获得系列IL-2突变体,并测定其免疫学活性和镇痛能力,发现无免疫学活性的IL-2突变体20Leu-IL-2仍具有中枢镇痛能力,而44Leu-IL-2,45 Val-IL-2虽保留了免疫学活性,但其镇痛能力显著性下降或消失,阿片受体拮抗剂纳洛酮能够阻断IL-2的中枢镇痛作用,而不能影响IL-2对CTLL-2细胞的增殖作用。抗内源性阿片肽血清与IL-2能发生明显的交叉反应。实验结果提示,IL-2分子是通过由第45位Tyr残基及空间上相近的Phe残基等组成的镇痛功能位点与阿片受体相结合而发挥镇痛效应。
The immunomodulatory factor interleukin-2 (IL-2) has central analgesic function. In the experiment, a series of IL-2 mutants were obtained by gene mutation technique and their immunological activity and analgesic ability were determined. It was found that 20Leu-IL-2, an immunologically inactive IL-2 mutant, still has central analgesic ability, 44Leu-IL-2,45 Val-IL-2 retains the immunological activity, but its analgesic ability significantly decreased or disappeared, the opioid receptor antagonist naloxone can block the central analgesic effect of IL-2, But could not affect the proliferation of CTLL-2 cells induced by IL-2. Anti-endogenous opioid peptide serum and IL-2 significant cross-reaction occurred. The experimental results suggest that the IL-2 molecule exerts the analgesic effect by binding the analgesic functional site consisting of the Tyr residue at position 45 and the Phe residue in space to opioid receptors.