Carr D J, Klimpel G R
J Neuroimmunol. 1986 Jul;12(1):75-87. doi: 10.1016/0165-5728(86)90099-8.
Previous reports have shown that endogenous opiates (beta-endorphin and met-enkephalin) have effects on cells of the immune system at physiologic concentrations. Using murine spleen cells, we herein report that beta-endorphin and met-enkephalin can enhance the generation of cytotoxic T lymphocytes (CTLs) at suboptimal concentrations of alloantigen in a one-way mixed lymphocyte culture (MLC). This enhancement is seen at levels ranging from 2.9 X 10(-8) M to 2.9 X 10(-14) M and 1.45 X 10(-6) M to 1.45 X 10(-12) M for beta-endorphin and met-enkephalin, respectively. This enhancement can be partially blocked by naloxone at 10(-7) M. Furthermore, the simultaneous addition of met-enkephalin and beta-endorphin does not increase the enhancement of CTL generation by either opiate peptide alone suggesting that they are acting through the same receptor. This report gives added proof for the regulatory-loop theory between the neuroendocrine and immune systems.
先前的报告表明,内源性阿片肽(β-内啡肽和甲硫氨酸脑啡肽)在生理浓度下对免疫系统细胞有影响。利用小鼠脾细胞,我们在此报告,在单向混合淋巴细胞培养(MLC)中,β-内啡肽和甲硫氨酸脑啡肽在次优浓度的同种异体抗原条件下可增强细胞毒性T淋巴细胞(CTL)的生成。β-内啡肽和甲硫氨酸脑啡肽分别在2.9×10⁻⁸ M至2.9×10⁻¹⁴ M和1.45×10⁻⁶ M至1.45×10⁻¹² M的浓度范围内可观察到这种增强作用。这种增强作用可被10⁻⁷ M的纳洛酮部分阻断。此外,同时添加甲硫氨酸脑啡肽和β-内啡肽并不会增强单独使用任一阿片肽时CTL生成的增强作用,这表明它们通过相同的受体起作用。本报告为神经内分泌系统和免疫系统之间的调节环路理论提供了更多证据。