The Notch signaling pathway regulates macrophage polarization in liver diseases.

The liver is not only the main metabolic site of exogenous compounds and drugs, but also an important immune organ in the human body. When a large number of nonself substances (such as drugs, alcohol, pathogens, microorganisms and their metabolites) enter the liver, they will cause serious liver diseases, including liver fibrosis, liver cirrhosis, liver failure, and hepatocellular carcinoma (HCC). Macrophages are the first line of defense against the invasion of exogenous pathogens and significant cellular components of the innate immune system.

miR-122-5p regulates hepatocytes damage caused by BaP and DBP co-exposure through SOCS1/STAT3 signaling in vitro.

BaP and DBP are ubiquitously and contemporaneously present in the environment. However, Current studies largely concentrate on the effects of a single pollutant (BaP or DBP). The liver is vital for biogenic activities.

DNMT1-mediated Foxp3 gene promoter hypermethylation involved in immune dysfunction caused by arsenic in human lymphocytes.

Growing evidence indicates that arsenic can cause long-lasting and irreversible damage to the function of the human immune system. It is known that forkhead box protein 3(Foxp3), which is specifically expressed in regulatory T cells (Tregs), plays a decisive role in immunoregulation and is regulated by DNA methylation. While evidence suggests that epigenetic regulated Foxp3 is involved in the immune disorders caused by arsenic exposure, the specific mechanism remains unclear.