Sprietsma J E
Med Hypotheses. 1997 Jul;49(1):1-14. doi: 10.1016/s0306-9877(97)90244-9.
Functional, excessive-possibly temporary-deficiencies of the trace element zinc can change immune functions prematurely from predominantly cellular Th1 responses to humoral Th2 responses. T helper (Th1) cells produce cytokines such as interleukin-2 (IL-2) and interferon gamma, thereby controlling viral infections and other intracellular pathogens more effectively than Th2 responses through cytokines such as IL-4, IL-5, IL-6 and IL-10. The accelerated shift from the production of extra Th1 cells during these cellular immune activities to more Th2 cells with their predominantly humoral immune functions, caused by such a zinc deficiency, adversely influences the course of diseases such as leprosy, schistosomiasis, leishmaniasis and AIDS, and can result in allergies. It is noteworthy that AIDS viruses (HIVs) do not replicate in Th1 cells, which probably contain more zinc, but preferentially in the Th0 and Th2 cells; all the more so, because zinc and copper ions are known to inhibit intracellular HIV replication. Considering the above Th1/Th2 switch, real prospects seem to be offered of vaccination against such parasites as Leishmania and against HIVs.
微量元素锌的功能性、过量（可能是暂时的）缺乏会过早地将免疫功能从以细胞介导的Th1反应为主转变为体液介导的Th2反应。辅助性T细胞（Th1）产生诸如白细胞介素-2（IL-2）和干扰素γ等细胞因子，因此与通过IL-4、IL-5、IL-6和IL-10等细胞因子介导的Th2反应相比，能更有效地控制病毒感染和其他细胞内病原体。由这种锌缺乏导致的在这些细胞免疫活动中从额外的Th1细胞产生向以体液免疫功能为主的更多Th2细胞的加速转变，会对麻风病、血吸虫病、利什曼病和艾滋病等疾病的病程产生不利影响，并可能导致过敏。值得注意的是，艾滋病病毒（HIV）不在可能含有更多锌的Th1细胞中复制，而是优先在Th0和Th2细胞中复制；更是如此，因为已知锌离子和铜离子会抑制细胞内HIV复制。考虑到上述Th1/Th2转换，针对利什曼原虫等寄生虫和HIV进行疫苗接种似乎具有切实的前景。
