Thymic atrophy, lymphopenia, and compromised cell- and antibody-mediated responses that cause increased rates of infections of longer duration are the immunological hallmarks of zinc deficiency (ZD) in humans and higher animals. As the deficiency advances, a reprogramming of the immune system occurs, beginning with the activation of the stress axis and chronic production of glucocorticoids that accelerate apoptosis among pre-B and -T cells. This reduces lymphopoiesis and causes atrophy of the thymus. In contrast, myelopoiesis is preserved, thereby providing protection for the first line of immune defense or innate immunity. Changes in gene expression for cytokines, DNA repair enzymes, zinc transporters, signaling molecules, etc., suggest that cells of the immune system are attempting to adapt to the stress of suboptimal zinc. Better understanding of the molecular and cellular changes made in response to inadequate zinc should lead to the development of immunotherapeutic interventions.

中文翻译：

---

锌缺乏时免疫系统的重新编程。

胸腺萎缩，淋巴细胞减少以及细胞和抗体介导的反应减弱（导致较长时间的感染率增加）是人类和高等动物中锌缺乏症（ZD）的免疫学标志。随着缺陷的发展，从应激轴的激活和糖皮质激素的长期产生开始，免疫系统发生重新编程，从而加速前B细胞和-T细胞之间的细胞凋亡。这减少了淋巴细胞生成并导致胸腺萎缩。相反，骨髓生成得以保留，从而为免疫防御或先天免疫的第一线提供保护。细胞因子，DNA修复酶，锌转运蛋白，信号分子等的基因表达变化表明，免疫系统的细胞正试图适应次优锌的胁迫。