嗜中性白血球參與發炎性疾病的機轉與角色
Neutrophils are the most abundant type of leukocyte in the circulation, responsible for immune surveillance, phagocytosing pathogens and the formation of extracellular traps to confine and kill pathogens. While neutrophils are dealing with diverse pathogens, self-metabolites such as immune complexes, advanced glycation end products (AGEs) and death-associates molecule patterns (DAMPs) can also trigger the formation of neutrophil extracellular traps (NETs). NETs elicited by those stimuli are associated with several inflammatory diseases such as systemic lupus erythematous (SLE), arthritis, and cardiovascular diseases. Those findings turn NETs from protective effects in host defense into detrimental impacts in chronic inflammation. Several studies have pinpointed the molecule mechanisms underlining the process of NET formation. However, understanding how pathogens and non-pathogenic stimuli induce NET formation, and the involvement of the innate immune receptors and regulators in the activation of NET formation, has remained an elusive goal. To address this gap, we are investigating the roles of NLRP12, an innate immune regulator belonging to the NOD-like superfamily, in regulating NET formation based on the platform we established (Nature Communications, 2017)..