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2017 ; 61
(6
): 687-697
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Host-pathogen interactions and subversion of autophagy
#MMPMID29233878
McEwan DG
Essays Biochem
2017[Dec]; 61
(6
): 687-697
PMID29233878
show ga
Macroautophagy ('autophagy'), is the process by which cells can form a
double-membraned vesicle that encapsulates material to be degraded by the
lysosome. This can include complex structures such as damaged mitochondria,
peroxisomes, protein aggregates and large swathes of cytoplasm that can not be
processed efficiently by other means of degradation. Recycling of amino acids and
lipids through autophagy allows the cell to form intracellular pools that aid
survival during periods of stress, including growth factor deprivation, amino
acid starvation or a depleted oxygen supply. One of the major functions of
autophagy that has emerged over the last decade is its importance as a safeguard
against infection. The ability of autophagy to selectively target intracellular
pathogens for destruction is now regarded as a key aspect of the innate immune
response. However, pathogens have evolved mechanisms to either evade or
reconfigure the autophagy pathway for their own survival. Understanding how
pathogens interact with and manipulate the host autophagy pathway will hopefully
provide a basis for combating infection and increase our understanding of the
role and regulation of autophagy. Herein, we will discuss how the host cell can
identify and target invading pathogens and how pathogens have adapted in order to
evade destruction by the host cell. In particular, we will focus on interactions
between the mammalian autophagy gene 8 (ATG8) proteins and the host and pathogen
effector proteins.
|Animals
[MESH]
|Autophagy-Related Protein 8 Family/genetics/metabolism
[MESH]