Szawlowski P W, Maddocks J L
Br J Clin Pharmacol. 1985 Aug;20(2):107-10. doi: 10.1111/j.1365-2125.1985.tb05039.x.
The effect of interleukin-2 on the response of the human MLR to azathioprine was studied. Azathioprine (36 microM) inhibited the MLR by 86% and interleukin-2 (25%) stimulated the MLR by 99%. Only partial relief (16%) of azathioprine (36 microM) inhibition was found in the interleukin-2 treated MLR compared with azathioprine treatment alone. However, [3H]-thymidine incorporation by azathioprine (36 microM) + interleukin-2 treated MLR was 4.3 times greater than that exposed to azathioprine alone. As the residual number of immunocompetent cells after drug exposure is pathologically more important than the fraction suppressed, this result may be of clinical relevance. These results show that the major mode of action of azathioprine is not the inhibition of interleukin-2 production.
研究了白细胞介素-2对人混合淋巴细胞反应（MLR）对硫唑嘌呤反应的影响。硫唑嘌呤（36微摩尔）使MLR抑制86%，而白细胞介素-2（25%）使MLR刺激99%。与单独使用硫唑嘌呤治疗相比，在经白细胞介素-2处理的MLR中，仅发现硫唑嘌呤（36微摩尔）抑制作用有部分缓解（16%）。然而，经硫唑嘌呤（36微摩尔）+白细胞介素-2处理的MLR中[3H] - 胸腺嘧啶核苷掺入量比仅暴露于硫唑嘌呤的情况大4.3倍。由于药物暴露后免疫活性细胞的残留数量在病理上比被抑制的比例更重要，该结果可能具有临床相关性。这些结果表明，硫唑嘌呤的主要作用方式不是抑制白细胞介素-2的产生。
