Spleen tyrosine kinase inhibition ameliorates airway inflammation through modulation of NLRP3 inflammosome and Th17/Treg axis

Schematic presentation of proposed mechanism of SYK inhibition mediated lung protection. β-Glucan acts through dectin-1 receptor activating tyrosine kinase (SYK) to further activate inflammasome components, causing inflammation. Inflammatory cytokines release IL-1β and recruit Th17 and neutrophils, causing lung damage. MNS, a potent SYK inhibitor, reduces lung damage via decreased Th17 and neutrophil expression. Meanwhile, the Treg population is increased through antigen-presenting cells by their cytokine milieu.207