Prasad A S, Beck F W, Grabowski S M, Kaplan J, Mathog R H
Department of Internal Medicine, Wayne State University School of Medicine, Detroit, MI, USA.
Proc Assoc Am Physicians. 1997 Jan;109(1):68-77.
Cell-mediated immune dysfunctions and susceptibility to infections have been observed in zinc-deficient human subjects. In this study, we investigated the production of cytokines and characterized the T-cell subpopulations in three groups of mildly zinc-deficient subjects. These included head and neck cancer patients, healthy volunteers who were found to have a dietary deficiency of zinc, and healthy volunteers in whom we induced zinc deficiency experimentally by dietary means. We used cellular zinc criteria for the diagnosis of zinc deficiency. We assayed enzyme-linked immunosorbent assay the production of cytokines from phytohemagglutinin-stimulated peripheral blood mononuclear cells and assessed by flow cytometry the differences in T-cell subpopulations. Our studies showed that the cytokines produced by TH1 cells were particularly sensitive to zinc status, inasmuch as the production of interleukin-2 (IL-2) and interferon-gamma were decreased even though the deficiency of zinc was mild in our subjects. TH2 cytokines (IL-4, IL-5, and IL-6) were not affected by zinc deficiency. Natural killer cell lytic activity also was decreased in zinc-deficient subjects. Recruitment of naive T cells (CD4+CD45 RA+) and CD8+ CD73+ CD11b-, precursors of cytolytic T cells, were decreased in mildly zinc-deficient subjects. An imbalance between the functions of TH1 and TH2 cells and changes in T-cell subpopulations are most probably responsible for cell-mediated immune dysfunctions in zinc deficiency.
在缺锌的人类受试者中已观察到细胞介导的免疫功能障碍和对感染的易感性。在本研究中，我们调查了三组轻度缺锌受试者的细胞因子产生情况，并对T细胞亚群进行了特征分析。这些受试者包括头颈癌患者、饮食中锌缺乏的健康志愿者，以及我们通过饮食方式实验性诱导锌缺乏的健康志愿者。我们使用细胞锌标准来诊断锌缺乏。我们通过酶联免疫吸附测定法检测了植物血凝素刺激的外周血单核细胞产生的细胞因子，并通过流式细胞术评估了T细胞亚群的差异。我们的研究表明，TH1细胞产生的细胞因子对锌状态特别敏感，因为即使我们的受试者锌缺乏程度较轻，白细胞介素-2（IL-2）和干扰素-γ的产生也会减少。TH2细胞因子（IL-4、IL-5和IL-6）不受锌缺乏的影响。缺锌受试者的自然杀伤细胞溶解活性也降低。轻度缺锌受试者中幼稚T细胞（CD4+CD45 RA+）和细胞毒性T细胞前体CD8+ CD73+ CD11b-的募集减少。TH1和TH2细胞功能之间的失衡以及T细胞亚群的变化很可能是锌缺乏时细胞介导的免疫功能障碍的原因。
