Macrophage Classical Activation

摘要: This chapter focuses on the critical steps of classical macrophage activation that have been emphasized by rare human diseases in which key components such as macrophages, are naturally deficient. In conjunction with other cells, macrophages will form granulomas. Numerous molecules definitely or putatively involved this process, and a few identified natural mutations. The author reviews these through an arbitrary artificial division proinflammatory response into premacrophage, intramacrophage, post-macrophage phases. activated TAK-1 activates IκB kinase (IKK) complex; complex is composed two catalytic subunits, IKK αand β, regulatory subunit IKKγ. Peripheral blood monocytes primary cultures from patients Wiskott-Aldrich syndrome (WAS) also demonstrate impaired FcγR-mediated phagocytosis due to defective phagocytic cup formation. Previous explanations for selective infection susceptibility chronic granulomatous disease (CGD) relied microbial catalase virulence factor. argument was that, whereas CGD phagocytes lacked superoxide hydrogen peroxide production, peroxide-producing microbes would complement defect cell unless they produced degrade their own peroxide. summary, neutrophils O2 - production. phagosome gradually acquires necessary lysosomal fusion produce phagolysosome. Defects degradation typically result intracellular accumulation undegraded substrates, characterized neurodegeneration without associated immunodeficiency. classically IFN-γ -primed recognizes, via specific surface receptors, products.