Department of Urinary Surgery, First Hospital of Bengbu Medical College, Bengbu 233000, Anhui Province, China.
Anhui Key Laboratory of Infection & Immunity, Bengbu Medical College, Bengbu 233000, Anhui Province, China.
Neural Regen Res. 2012 Dec 15;7(35):2811-7. doi: 10.3969/j.issn.1673-5374.2012.35.009.
Bone marrow precursor cells were extracted from C57BL/6J mice aged 7-8 weeks, and dendritic cells were purified using anti-CD11c (a specific marker for dendritic cells) antibody-coated magnetic beads. Immunofluorescence staining revealed that the expression levels of endomorphin-1 and endomorphin-2 were upregulated in dendritic cells activated by lipopolysaccharide. An enzyme immunoassay showed that lipopolysaccharide and other Toll-like receptor ligands promoted the secretion of endomorphin-1 and endomorphin-2 from activated dendritic cells. [(3)H]-thymidine incorporation demonstrated that endomorphin-1 and endomorphin-2 both inhibited the proliferation of T lymphocyte induced by activated dendritic cells. Furthermore, this immunosuppressive effect was blocked by CTOP, a specific antagonist of µ-opioid receptors. Our experimental findings indicate that activated dendritic cells can induce the expression and secretion of endomorphins, and that endomorphins suppress T lymphocyte proliferation through activation of µ-opioid receptors.
从 7-8 周龄 C57BL/6J 小鼠中提取骨髓前体细胞，使用抗 CD11c（树突状细胞的特异性标志物）抗体包被的磁珠纯化树突状细胞。免疫荧光染色显示，脂多糖激活的树突状细胞中内吗啡肽-1 和内吗啡肽-2 的表达水平上调。酶免疫分析显示，脂多糖和其他 Toll 样受体配体促进激活的树突状细胞分泌内吗啡肽-1 和内吗啡肽-2。[(3)H]-胸苷掺入表明内吗啡肽-1 和内吗啡肽-2 均可抑制由激活的树突状细胞诱导的 T 淋巴细胞增殖。此外，这种免疫抑制作用可被 µ-阿片受体的特异性拮抗剂 CTOP 阻断。我们的实验结果表明，激活的树突状细胞可诱导内吗啡肽的表达和分泌，并且内吗啡肽通过激活 µ-阿片受体抑制 T 淋巴细胞增殖。
