PKC θ-mediated Ca2+/NF-AT signalling pathway may be involved in T-cell immunosuppression in coal-burning arsenic-poisoned population.

Abstract

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 Ca2+/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.

• Authors: Qibing Zeng, Peng Luo, Junying Gu, Bing Liang, Qizhan Liu, Aihua Zhang
• Journal: Environmental toxicology and pharmacology (Environ Toxicol Pharmacol) Vol. 55 Pg. 44-50 (Oct 2017) ISSN: 1872-7077 [Electronic] Netherlands
• PMID: 28823652 (Publication Type: Journal Article)
• Copyright: Copyright © 2017 Elsevier B.V. All rights reserved.

Chemical References

• Coal
• IFNG protein, human
• IL2 protein, human
• Interleukin-2
• NFATC Transcription Factors
• Interferon-gamma
• PRKCQ protein, human
• Protein Kinase C-theta
• Calcium

Topics

• Adult
• Arsenic Poisoning (genetics, immunology, metabolism)
• Calcium (metabolism)
• Cell Proliferation (drug effects)
• Cells, Cultured
• Coal (adverse effects)
• Female
• Gene Expression Regulation (drug effects)
• Humans
• Interferon-gamma (genetics)
• Interleukin-2 (genetics)
• Male
• Middle Aged
• NFATC Transcription Factors (metabolism)
• Phosphorylation (drug effects)
• Protein Kinase C-theta (metabolism)
• Signal Transduction
• T-Lymphocytes (cytology, drug effects)