IL-17A Promotes Intracellular Growth of Mycobacterium by Inhibiting Apoptosis of Infected Macrophages

摘要: The fate of infected macrophages is a critical aspect immunity to mycobacteria. By depriving the pathogen its intracellular niche, apoptotic death macrophage has been shown be an important mechanism control bacterial growth. Here, we show that IL-17 inhibits apoptosis Mycobacterium bovis BCG- or tuberculosis-infected thus hampering their ability Mechanistically, p53, and impacts on intrinsic pathway, by increasing Bcl2 decreasing Bax expression, cytochrome c release from mitochondria, inhibiting caspase-3 activation. same effect was observed in upon blockade p53 nuclear translocation. These results reveal previously unappreciated role for IL-17/p53 axis regulation mycobacteria-induced can have implications broad spectrum diseases where cell host defense mechanism.