Key Laboratory of Environmental Pollution Monitoring and Disease Control, Ministry of Education, Department of Toxicology, Guizhou Medical University, Guiyang 550025, Guizhou, China.
The Key Laboratory of Modern Toxicology, Ministry of Education, School of Public Health, Nanjing Medical University, Nanjing 211166, Jiangsu, China.
Environ Toxicol Pharmacol. 2017 Oct;55:44-50. doi: 10.1016/j.etap.2017.08.005. Epub 2017 Aug 12.
Arsenic poisoning is a worldwide endemic disease that affects thousands of people. Growing evidence from animal, cell, and human studies indicates that arsenic has deleterious effects on the immune system. The present investigation is a population-based study that observed changes in the proliferation of human T-cells and IL-2 and INF-γ mRNA expression. Our results show that coal-burning arsenic can cause T-cell immunosuppression in the population, and participates in the occurrence and development of arsenic poisoning. In addition, we analyzed the intracellular calcium index, expression of protein kinase C theta (PKC θ) and phosphorylated PKC θ, and the DNA-binding activity of NF-AT in peripheral blood mononuclear cells (PBMCs). Our analysis demonstrates that the PKC θ-mediated Ca/NF-AT signalling pathway may be involved in the T-cell immunosuppression of coal-burning arsenic-poisoned population. This study provides important data for a mechanistic understanding of endemic arsenic poisoning.
砷中毒是一种全球性地方病,影响着成千上万的人。越来越多的动物、细胞和人体研究证据表明,砷对免疫系统有有害影响。本研究是一项基于人群的研究,观察了人 T 细胞增殖以及 IL-2 和 INF-γ mRNA 表达的变化。我们的结果表明,燃煤砷会导致人群 T 细胞免疫抑制,并参与砷中毒的发生和发展。此外,我们还分析了细胞内钙指数、蛋白激酶 C 理论(PKCθ)和磷酸化 PKCθ的表达,以及外周血单个核细胞(PBMC)中 NF-AT 的 DNA 结合活性。我们的分析表明,PKCθ 介导的 Ca/NF-AT 信号通路可能参与了燃煤砷中毒人群 T 细胞免疫抑制。这项研究为了解地方性砷中毒的发病机制提供了重要数据。