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抗ＩＬ－２受体α亚基的单克隆抗体不能阻断ＩＬ－２的中枢镇痛作用，以及丧失与ＩＬ－２受体β亚基结合能力的ＩＬ－２突变体仍具有提高大鼠痛阈的能力，这表明ＩＬ－２的中枢镇痛作用并不是通过ＩＬ－２受体所介导，亦表示ＩＬ－２的免疫和镇痛作用是通过不同的受体途径实现的。加之内源性阿片肽与ＩＬ－２分子有着共同的抗原决定基和结构相似性，提示ＩＬ－２可以与阿片受体直接结合产生中枢镇痛效应。从放射免疫法测定的ＩＬ－２侧脑室注射后不同时间大鼠脑内不同核团的内源性阿片肽含量，推测ＩＬ－２的中枢镇痛作用可能还与弓状核、室旁核、蓝斑等核团的β－ＥＰ和ＬＥＫ有关。
Monoclonal antibodies against the alpha subunit of IL-2 receptor do not block the central analgesic effect of IL-2 and IL-2 mutants that lose their ability to bind to the beta subunit of IL-2 receptor still have the effects of increasing rat pain Threshold, indicating that the central analgesic effect of IL-2 is not mediated by IL-2 receptors and that the immune and analgesic effects of IL-2 are mediated through different receptor pathways. Combined with endogenous opioid peptides and IL-2 molecules have a common epitope and structural similarity, suggesting that IL-2 and opioid receptors can produce direct central analgesic effect. The levels of endogenous opioid peptides in different nuclei of rat brain at different time points after intracerebroventricular injection of IL-2 measured by radioimmunoassay suggested that the central analgesic effect of IL-2 may be related to arcuate nucleus, paraventricular nucleus, Plaques and other nuclei of the β-EP and LEK related.