ABSTRACT
Programmed death-ligand 1 (PD-L1) is important in maintaining central and peripheral immune tolerance in normal tissues, mediating tumor immune escape and keeping the balance between anti- and pro-inflammatory responses. Inflammation plays an important role in inflammatory lung diseases. This article reviews the research progress and potential clinical value of PD-L1 in inflammatory lung diseases, including acute lung injury, chronic obstructive pulmonary disease, asthma and idiopathic pulmonary fibrosis.
Subject(s)
Asthma , B7-H1 Antigen , Pulmonary Disease, Chronic Obstructive , Humans , B7-H1 Antigen/metabolism , B7-H1 Antigen/immunology , Pulmonary Disease, Chronic Obstructive/immunology , Asthma/immunology , Acute Lung Injury/immunology , Inflammation/immunology , Idiopathic Pulmonary Fibrosis/immunology , Idiopathic Pulmonary Fibrosis/metabolism , Lung Diseases/immunology , Lung Diseases/metabolism , AnimalsABSTRACT
Titanium dioxide nanoparticles (TiO2 NPs) are massively produced and widely used in daily life, which may pose potential risk to human health via uncharacterized interaction between DNAs. This research aims to examine the interaction between DNA and three types of TiO2 NPs of different sizes and crystallines. The interaction between TiO2 NPs and liver DNA molecules obtained from Sprague-Dawley rats was systematically evaluated in vivo using atomic force microscopy, transmission electron microscopy, various spectroscopic techniques and gel electrophoresis. We found that TiO2 NPs (diameter <25 nm and <100 nm) in anatase crystalline can covalently interact with liver DNA by either inserting itself in between DNA base pairs or binding to DNA nucleotide via P-O-Ti-O bond. Such interaction may not be NP size-dependent but may be crystalline phase-dependent, because such interaction did not occur in rutile crystal phase, in which the DNA damage was potentially caused by reactive oxygen species.