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2016 ; 23
(6
): 990-6
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Exploiting death: apoptotic immunity in microbial pathogenesis
#MMPMID26943319
Ucker DS
Cell Death Differ
2016[Jun]; 23
(6
): 990-6
PMID26943319
show ga
Innate immunity typically is responsible for initial host responses against
infections. Independently, nucleated cells that die normally as part of the
physiological process of homeostasis in mammals (including humans) suppress
immunity. Specifically, the physiological process of cell death (apoptosis)
generates cells that are recognized specifically by viable cells of all types and
elicit a profound transient suppression of host immunity (termed 'innate
apoptotic immunity' (IAI)). IAI appears to be important normally for the
maintenance of self-tolerance and for the resolution of inflammation. In
addition, pathogens are able to take advantage of IAI through a variety of
distinct mechanisms, to enable their proliferation within the host and enhance
pathogenicity. For example, the protist pathogen Leishmania amazonensis, at its
infective stage, mimics apoptotic cells by expressing apoptotic-like protein
determinants on the cell surface, triggering immunosuppression directly. In
contrast, the pathogenic bacterium Listeria monocytogenes triggers cell death in
host lymphocytes, relying on those apoptotic cells to suppress host immune
control and facilitate bacterial expansion. Finally, although the inhibition of
apoptotic cell death is a common attribute of many viruses which facilitates
their extended replication, it is clear that adenoviruses also reprogram the
non-apoptotic dead cells that arise subsequently to manifest apoptotic-like
immunosuppressive properties. These three instances represent diverse strategies
used by microbial pathogens to exploit IAI, focusing attention on the potency of
this facet of host immune control. Further examination of these cases will be
revealing both of varied mechanisms of pathogenesis and the processes involved in
IAI control.
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