한빛사논문
- 조회941
Dong Sun Oh1, Jang Hyun Park1, Hi Eun Jung1, Hyun-Jin Kim1, Heung Kyu Lee1,2,*
1Graduate School of Medical Science and Engineering, Korea Advanced Institute of Science and Technology (KAIST) , Daejeon 34141, Republic of Korea.
2The Center for Epidemic Preparedness, KAIST Institute, KAIST , Daejeon 34141, Republic of Korea.
*Corresponding author
Abstract
Respiratory syncytial virus (RSV) is a leading cause of respiratory tract infections in infants. Macroautophagy/autophagy is a catalytic metabolic process required for cellular homeostasis. Although intracellular metabolism is important for immune responses in dendritic cells, the link between autophagy and immunometabolism remains unknown. Here, we show that the autophagy-related protein ATG5 regulates immunometabolism. Atg5-deficient mouse dendritic cells showed increased CD8A+ T-cell response and increased secretion of proinflammatory cytokines upon RSV infection. Transcriptome analysis showed that Atg5 deficiency alters the expression of metabolism-related genes. Atg5-deficient dendritic cells also showed increased activation of glycolysis and the AKT-MTOR-RPS6KB pathway and decreased mitochondrial activity, all of which are cellular signatures for metabolic activation. These cells also showed elevated CD8A+ T-cell priming and surface major histocompatibility complex (MHC) class I expression. Our results suggested that ATG5 regulated host immune responses by modulating dendritic cell metabolism. These findings may help develop potential antiviral therapies that alter host immunity by regulating autophagy and immunometabolism.
논문정보
- Research article
- 2020년 08월 (BRIC 등록일 2020-08-26)
- 국내 연구진
- 생명과학 > 면역학
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