Fig. 5
Schematic graph illustrating the association of both Ncf1 and Nos2 with MOG peptide-induced EAE. The Ncf1-mediated regulation was associated with IL-1β secreted by neutrophils in the response to pertussis toxin in mice during the early stage of EAE development. aNcf1 mutation impaired ROS production by the NOX2 complex, decreased IL-1β production by neutrophils, and reduced EAE in Nos2-sufficient mice. bNcf1 mutation enhanced IL-1β production by neutrophils and increased EAE in Nos2-deficient mice that failed to produce nitric oxide. NOS2 deficiency enhanced EAE in the chronic phase, irrespective of Ncf1 status. c TNF-α production was increased in response to MOG79-96 stimulation in Ncf1-Nos2-deficient mice after immunization. In summary, a potential mechanism underlying the interaction between neutrophils and T cells might regulate the EAE development in an NCF1-NOS2-dependent manner