Zinc status in human immunodeficiency virus infection
Zinc status in human immunodeficiency virus infection
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DOI：
10.1093/jn/130.5.1421s
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发表时间：
2000-05-01
影响因子：
4.2
通讯作者：
Campa, A
中科院分区：
文献类型：
--
作者：
Baum, MK;Shor-Posner, G;Campa, A
有大量证据支持锌在免疫过程中的重要作用。充足的锌状态对于 T 细胞分裂、成熟和分化至关重要；淋巴细胞对有丝分裂原的反应；淋巴和骨髓来源的程序性细胞死亡；基因转录；和生物膜功能。淋巴细胞是被锌激活的细胞类型之一，锌是多种蛋白质、神经肽、激素受体和多核苷酸的结构成分。最著名的锌依赖性激素/酶包括铜、锌超氧化物歧化酶（抗氧化防御系统的酶成分）和胸腺素（对于 T 淋巴细胞的形成至关重要）。在动物和人类中，缺锌会导致胸腺快速明显萎缩、细胞介导的皮肤敏感性受损和淋巴细胞减少。缺锌时，一抗和二抗反应会减少，特别是对于那些需要 T 细胞帮助的抗原，例如异源红细胞中的抗原。此外，免疫后抗体反应和脾细胞毒性 T 细胞的生成也会减少。锌还能抑制肿瘤坏死因子的产生，肿瘤坏死因子与获得性免疫缺陷综合征中恶病质和消瘦的病理生理学有关。
There is substantial evidence to support an important role for zinc in immune processes. Adequate zinc status is essential for T-cell division, maturation and differentiation; lymphocyte response to mitogens; programmed cell death of lymphoid and myeloid origins; gene transcription; and biomembrane function. Lymphocytes are one of the types of cells activated by zinc, Zinc is the structural component of a wide variety of proteins, neuropeptides, hormone receptors and polynucleotides. Among the best known zinc-dependent hormones/enzymes are Cu, Zn superoxide dismutase, an enzyme component of the antioxidant defense system, and thymulin, which is essential for the formation of T-lymphocytes. In animals and humans, zinc deficiency results in rapid and marked atrophy of the thymus, impaired cell-mediated cutaneous sensitivity and lymphopenia. Primary and secondary antibody responses are reduced in zinc deficiency, particularly for those antigens that require T-cell help, such as those in heterologous red blood cells, In addition, antibody response and the generation of splenic cytotoxic T cells after immunization are reduced. Zinc also inhibits the production of tumor necrosis factor, which is implicated in the pathophysiology of cachexia and wasting in acquired immune deficiency syndrome.