NOX2-deficient neutrophils facilitate joint inflammation in immune-mediated arthritis though higher proinflammatory and weakened immune checkpoint activities

The cellular and molecular factors contributing to the joint inflammation in different redox conditions have not been clearly elucidated. Previous research showed that phagocyte-produced reactive oxygen species (ROS) play an anti-inflammatory role in K/BxN serum-induced arthritis and NOX2-deficient mice tend to have more severe arthritis. However, the role of neutrophils, which are the main producers of ROS in inflammation, is still unclear. In this study, we assessed the immunomodulatory function of neutrophils from arthritic joints of NOX2-deficient and wild type mice.