作者: Steven M. Debol , Michael J. Herron , Robert D. Nelson
DOI: 10.1002/JLB.62.6.827
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摘要: Dapsone has clinical utility as an anti-inflammatory agent but the mechanism of this action remains unknown. We have previously reported that dapsone inhibits beta2 integrin (CD11b/CD18)-mediated adherence human neutrophils in vitro and now describe studies designed to discover how dapsone-mediated inhibition neutrophil function occurs. Results indicate interferes with activation or G-protein (Gi type) initiates signal transduction cascade common chemotactic stimuli. They also show suppression pathway generation second messengers essential molecules, well respiratory secretory functions exposed chemoattractants. propose chemoattractant-induced by suppresses recruitment local production toxic products affected skin dermatitis herpetiformis other neutrophilic dermatoses.