Rodríguez L, Graniel J, Ortiz R
Universidad Autónoma Metropolitana-Iztapalapa, Departamento de Ciencias de la Salud, Mexico.
Clin Exp Immunol. 2007 Jun;148(3):478-85. doi: 10.1111/j.1365-2249.2007.03361.x. Epub 2007 Mar 9.
Malnutrition compromises immune function, resulting in reduced resistance to infection. Recent animal and human studies have suggested that leptin is capable of modulating the immune response and that its levels, which are regulated by nutritional status, fall rapidly during starvation. Leptin deficiency is associated with impaired cell-mediated immunity, an increased incidence of infectious disease and an associated increase in mortality. The purpose of this study was to examine the effect of leptin on activation and cytokine production in peripheral blood T cells from malnourished children. The data obtained in the present study demonstrate that leptin produced an increase in the percentage of CD4(+) and CD8(+) cells producing interleukin (IL)-2 and interferon (IFN)-gamma in 24-h cultures. Moreover, leptin decreased the percentage of CD4(+) and CD8(+) cells producing IL-4 and IL-10, and enhanced activation of circulating T cells when co-stimulated by phorbol 12-myristate 13 acetate (PMA)-ionomycin. Leptin enhanced the expression of activation markers CD69 and CD25 in both CD4(+) and CD8(+) cells after 5 h of stimulation. In conclusion, the results obtained show that leptin modulates CD4(+) and CD8(+) cell activation towards a T helper 1 (Th1) phenotype by stimulating the synthesis of IL-2 and IFN-gamma. In contrast, leptin decreases IL-4 and IL-10 production. Moreover, leptin enhanced the expression of CD69 and CD25 on CD4(+) and CD8(+) cells after stimulation with PMA-ionomycin.
营养不良会损害免疫功能,导致抗感染能力下降。最近的动物和人体研究表明,瘦素能够调节免疫反应,且其水平受营养状况调控,在饥饿期间会迅速下降。瘦素缺乏与细胞介导的免疫功能受损、传染病发病率增加以及死亡率上升有关。本研究的目的是检测瘦素对营养不良儿童外周血T细胞激活及细胞因子产生的影响。本研究获得的数据表明,在24小时培养中,瘦素使产生白细胞介素(IL)-2和干扰素(IFN)-γ的CD4(+)和CD8(+)细胞百分比增加。此外,瘦素降低了产生IL-4和IL-10的CD4(+)和CD8(+)细胞百分比,并在佛波醇12-肉豆蔻酸酯13-乙酸酯(PMA)-离子霉素共同刺激时增强了循环T细胞的激活。刺激5小时后,瘦素增强了CD4(+)和CD8(+)细胞中激活标志物CD69和CD25的表达。总之,所获结果表明,瘦素通过刺激IL-2和IFN-γ的合成,将CD4(+)和CD8(+)细胞激活调节为T辅助细胞1(Th1)表型。相比之下,瘦素减少IL-4和IL-10的产生。此外,在PMA-离子霉素刺激后,瘦素增强了CD4(+)和CD8(+)细胞上CD69和CD25的表达。