A high number of illnesses and disorders are connected to zinc deficiency. Equally, T cell polarization and a balance between different T helper (Th) cell subsets are essential. Therefore, in this study, the influence of zinc deficiency on T cell polarization and on respective signaling pathways was investigated. We uncovered a significantly increased number of regulatory T cells (Treg) and Th17 cells in expanded T cells during zinc deficiency after 3 days of combined treatment with IL-2 and TGF-β1 (Treg) or IL-6 and TGF-β1 (Th17). No difference in Th1 and Th2 cell polarization between zinc-deficient and zinc-adequate status was prominent. On the molecular level, Smad signaling was significantly enhanced by stimulation with TGF-β1/IL-6 during zinc deficiency compared to adequate zinc condition. This represents an explanation for the elevated Th17 cell numbers associated with autoimmune disease especially during zinc deficiency. Moreover, Treg cell numbers are increased during zinc deficiency as well. However, those cells might be nonfunctional since a lower expression of miR-146a was uncovered compared to normal zinc concentrations. In summary, an adequate zinc homeostasis is fundamental to slow down or probably stop the progression of autoimmune diseases and infections. Therefore, supplementing zinc might be a therapeutic approach to dampen autoimmune diseases connected to Th17 cells.

大量疾病和失调与锌缺乏症有关。同样，T细胞极化和不同T辅助（Th）细胞子集之间的平衡至关重要。因此，在这项研究中，研究了锌缺乏对T细胞极化和各自信号通路的影响。在用IL-2和TGF-β1（Treg）或IL-6和TGF-β1（Th17）联合治疗3天后，我们发现在锌缺乏期间扩增的T细胞中调节性T细胞（Treg）和Th17细胞的数量明显增加）。锌缺乏和锌充足状态之间的Th1和Th2细胞极化无明显差异。在分子水平上，与充足的锌条件相比，在缺锌期间通过TGF-β1/ IL-6刺激可以显着增强Smad信号传导。这代表了与自身免疫性疾病相关的Th17细胞数量增加的解释，尤其是在锌缺乏时。此外，在锌缺乏期间，Treg细胞数量也增加。但是，由于未发现与正常锌浓度相比更低的miR-146a表达，因此这些细胞可能没有功能。总之，充足的锌稳态对减慢或可能阻止自身免疫性疾病和感染的进展至关重要。因此，补充锌可能是减轻与Th17细胞有关的自身免疫性疾病的治疗方法。这些细胞可能没有功能，因为未发现与正常锌浓度相比更低的miR-146a表达。总之，充足的锌稳态对减慢或可能阻止自身免疫性疾病和感染的进展至关重要。因此，补充锌可能是减轻与Th17细胞有关的自身免疫性疾病的治疗方法。这些细胞可能没有功能，因为未发现与正常锌浓度相比更低的miR-146a表达。总之，充足的锌稳态对减慢或可能阻止自身免疫性疾病和感染的进展至关重要。因此，补充锌可能是减轻与Th17细胞有关的自身免疫性疾病的治疗方法。