Yoshii H, Kawakubo H, Matsuoka T, Suehiro S, Yanagihara Y, Negoro S, Kishimoto S
Department of Hematology and Immunology, Nippon Zoki Pharmaceutical Company, Hyogo, Japan.
Int J Immunopharmacol. 1991;13(7):859-64. doi: 10.1016/0192-0561(91)90037-8.
In a previous paper, we have demonstrated that Neurotropin, a non-protein extract isolated from the inflamed skin of rabbits inoculated with vaccinia virus, restores decreasing immune responses through the recovery of interleukin-2 (IL-2) production in aging BALB/c mice. To clarify the mechanism by which Neurotropin restores IL-2 production, its effect on the recruitment of IL-2-producing T-cells from bone marrow cells was examined using syngenic radiation bone marrow chimeras. Two fundamental lesions in recruiting IL-2-producing T-cells in aging BALB/c mice were demonstrated: (1) a drastic decline of the maturation of bone marrow cells to IL-2-producing T-cells as demonstrated by old----young chimeras; and (2) an environment unable to support bone marrow cell differentiation to IL-2-producing T-cells by young----old chimeras. Neurotropin clearly restored the maturation of bone marrow cells to IL-2-producing T-cells when administered from 13 to 16 month-old mice, whereas the non-complementing environment was not normalized with Neurotropin administration. These results suggest that Neurotropin administration restores IL-2 production through the recovery of the maturation of bone marrow cells to IL-2-producing T-cells, resulting in restoration of in vivo T-cell immune response in aging BALB/c mice.
在之前的一篇论文中,我们已经证明,神经妥乐平(一种从接种痘苗病毒的兔子发炎皮肤中分离出的非蛋白质提取物)可通过恢复衰老的BALB/c小鼠白细胞介素-2(IL-2)的产生来恢复下降的免疫反应。为了阐明神经妥乐平恢复IL-2产生的机制,我们使用同基因辐射骨髓嵌合体研究了其对从骨髓细胞中募集产生IL-2的T细胞的影响。研究发现衰老的BALB/c小鼠在募集产生IL-2的T细胞方面存在两个基本缺陷:(1)如老年-年轻嵌合体所示,骨髓细胞向产生IL-2的T细胞成熟的急剧下降;(2)如年轻-老年嵌合体所示,存在一个无法支持骨髓细胞分化为产生IL-2的T细胞的环境。当对13至16月龄的小鼠给药时,神经妥乐平明显恢复了骨髓细胞向产生IL-2的T细胞的成熟,而给药神经妥乐平并未使非互补环境恢复正常。这些结果表明,给药神经妥乐平可通过恢复骨髓细胞向产生IL-2的T细胞的成熟来恢复IL-2的产生,从而恢复衰老的BALB/c小鼠体内的T细胞免疫反应。