期刊
CELL HOST & MICROBE
卷 22, 期 2, 页码 166-175出版社
CELL PRESS
DOI: 10.1016/j.chom.2017.07.005
关键词
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资金
- Fonds de Recherche du Quebec - Sante (FRQS) [33790]
- NIH [1P01 AI063302, 1R01 AI027655, R01 AI110684, RO1 AI113211]
Recent excitement regarding immune clearance of intracellular microorganisms has focused on two systems thatmaintain cellular homeostasis. One system includes cellular autophagy components that mediate degradation of pathogens in membrane-bound compartments, in a process termed xenophagy. The second system is driven by interferon-regulated GTPases that promote rupture of pathogen-containing vacuoles and microbial degradation. In the case of xenophagy, pathogen sequestration and compartmentalization suppress inflammation. In contrast, interferon-driven events can lead to exposure of pathogen-associated molecular patterns to the host cytosol with consequent inflammasome activation. Paradoxically, signals and factors involved in xenophagy also mobilize interferon-regulated GTPases, which drive the inflammatory response, indicating considerable cross-talk between these pathways. How these responses are prioritized remains to be understood. In this review, we describe mechanisms of intracellular pathogen clearance that rely on the autophagy machinery and interferon-regulated GTPases, and speculate how these pathways engage each other to balance pathogen elimination with inflammation.
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