Tuberc Respir Dis > Volume 65(4); 2008 > Article
Tuberculosis and Respiratory Diseases 2008;65(4):343-350.
DOI: https://doi.org/10.4046/trd.2008.65.4.343    Published online October 1, 2008.
Induction Mechanism of PD-L1 (Programmed Cell Death-ligand 1) in Sepsis.
Sang Min Lee
Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine and Lung Institute, Medical Research Center, Seoul National University College of Medicine, Seoul, Korea. sangmin2@snu.ac.kr
Abstract
PD-L1 is expressed in a variety of antigen-presenting cells and provides T cell tolerance via ligation with its receptor PD-1 and B7-1 on T cells. Stimulation with lipopolysaccharide (LPS) can increase the level of PD-L1 expression in B cells and macrophages, which suggests that this molecule plays a role in the immunosuppression observed in severe sepsis. The aim of this study was to identify which of the downstream pathways of TLR4 are involved in the up-regulation of PD-L1 by LPS in macrophages. Flow cytometry was used to examine the expression of PD-L1 in RAW 264.7 macrophages stimulated with LPS. The following chemical inhibitors were used to evaluate the role of each pathway: LY294002 for PI3K/Akt, SB202190 for p38 MAPK, and U0126 for MEK. LPS induced the expression of PD-L1 in a time- and dose-dependent manner. Transfection of siRNA for TLR4 suppressed the induction of PD-L1. Pretreatment with LY294002 and SB202190 decreased the level of PD-L1 expression but U0126 did not. Overall, the PI3K/Akt and p38 MAPK pathways are involved in the up-regulation of PD-L1 expression in RAW 264.7 macrophages stimulated with LPS.
Key Words: PD-L1, LPS, Sepsis, Macrophage
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