IL-33 Deficiency Attenuates Lung Inflammation by Inducing Th17 Response and Impacting the Th17/Treg Balance in LPS-Induced ARDS Mice via Dendritic Cells.
Li ChengYang JiaoWei JiangXin ZhangLiping ZhangGongwei JiaPublished in: Journal of immunology research (2022)
IL-33 deficiency alleviated lung injury in the LPS-induced ARDS model, which was closely related to suppressing Th17 responses and regulating the Th17/Treg balance. The expansion of Th17 cells and imbalance in Th17/Treg cells may be associated with IL-6 and IL-23 secreted from IL-33-activated DCs.
Keyphrases
- lps induced
- inflammatory response
- induced apoptosis
- dendritic cells
- cell cycle arrest
- acute respiratory distress syndrome
- oxidative stress
- immune response
- extracorporeal membrane oxygenation
- mechanical ventilation
- cell death
- signaling pathway
- type diabetes
- intensive care unit
- metabolic syndrome
- skeletal muscle
- endoplasmic reticulum stress
- regulatory t cells
- pi k akt